Giovanni Boccacccio’s The Decameron consists of a collection of short stories written around 1350, just after the Bubonic Plague swept China, India, Persia, Syria, Egypt, and Europe, eventually killing an estimated 60% of the European population, primarily of peasant stock, which indirectly affected the food supply, since this was the population that cultivated the land and grew the food. In the book’s introduction, the author presents a fairly clear picture of how people nearly 700 years ago reacted to the pandemic. While the disease was of somewhat mysterious origin and would have produced the perception that the population had fallen under some form of Divine judgment, they were certainly aware that it was contagious and that person-to-person transmission was taking place. “There were some people who thought that living modestly and avoiding excess might help a great deal in resisting the disease,” Boccaccio wrote. “So they gathered in small groups and lived entirely apart from everyone else. They shut themselves up in those houses where one could live well.” They created a bubble around themselves and adopted shelter-in-place measures similar to today’s CoViD-19 lockdown practices.
“Others thought the opposite: they believed that drinking excessively, enjoying life, going about singing and celebrating, satisfying in every way the appetites as best they could, laughing, and making light of everything by going to one tavern to another all day and night,” Boccaccio wrote, was the best antidote. They were probably wrong, but their modern equivalent, those who defy the lockdown and party and refuse to maintain social distancing are probably wrong too. Others adopted the middle way. They did not attend bacchanals, nor did they quarantine themselves. “They went about carrying in their hand’s flowers, or sweet-smelling herbs, or various kinds of spices; and they held them to their noses, believing such smells were a wonderful means of purifying the brain,” Boccaccio wrote. They would be the equivalent of those who turn to alternative medicine to cure their ills. “Others were of a crueler opinion; they maintained that there was no better medicine than to flee and men and women in great numbers abandoned their city, their houses, and their relatives.” Boccaccio wrote that fear so gripped the population that people even felt compelled to abandon their loved ones. “Brother abandoned brother, uncle abandoned nephew and very often wife abandoned husband.” Parents were even known to abandon their children. Today, at the height of the crisis, the cruelty of isolation has certainly been felt by the elderly and the infected, with relatives kept away, regardless of their wish or intention.i
Certainly, medical knowledge back in the days of Boccaccio is a far cry from what it is today, but with vaccines being the only antidote that officialdom will acknowledge or accept, with all other antidotes being suppressed, it is clear that the scientific dictatorship limits our options in fighting this disease with as hard-headed, arrogant, and obdurate a stance as our medieval forebears. We really haven’t advanced as a society nor as a scientific community one iota. We just like to pretend we have, and the pretense wears thin rather quickly as it becomes more and more apparent that our medical tsars wear no clothes and are standing before us stark naked.
In times of plague, whether its invasive species like locusts, murder hornets, killer bees, lamprey eel or carp, or whether its plagues like HIV/AIDS or strains of the flu, there is a tendency to blame them all on foreigners and give them foreign names, because the source of all plagues seems to be the “other,” all those who are not as we are. Hence, CoViD-19 was originally dubbed the China virus or the Wuhan Flu. But this is not the only time, flu bugs have been given foreign names. There have been an array of these foreign-sounding plagues over the course of the 20th century like the Hong Kong Flu or the Spanish Flu of 1918 for instance. The so-called Spanish Flu actually began life in the U.S. but was variously known in other countries as the German Flu, the French Flu, the Brazilian Flu, but finally ended up being recorded in history books as the Spanish Flu. Some records suggest the Spanish Flu infected more than half of the 2 billion inhabitants living at the time.
The Spanish flu infected greater than 50% of Earth’s inhabitants and is thought to have been responsible for as many as 50 million deaths worldwide. To make matters worse, it hit near the end of the Great War, which was responsible for eviscerating 40 million soldiers and civilians from the face of the planet in what had to be the cruelest combat zone ever known. By the time the Armistice was signed, the pandemic was riding the second wave of a disease tsunami that went around the world.ii
The CoViD-19 variant now sweeping the world is subtly different from the one that first emerged in China. SARS-Cov-2 is the official name of the virus known under the informal name CoViD-19. The infectious disease that is continuing to spread around the globe is undergoing mutations at a mercurial pace. However, while scientists have taken stock of thousands of mutations, or changes to the virus’s genetic makeup, one variant, in particular, that emerged late in 2020, has raised the alarm.
The crucial questions about this mutation are: does this make the virus more pathogenic or virulent or both? And could it undermine efforts by vaccine-makers to come up with an effective vaccine against the first strain? This coronavirus is actually changing very slowly compared with a virus like the common flu. With relatively low levels of natural immunity in the population, no vaccine and few effective treatments, there is nothing to serve as a catalyst for it to mutate or attempt to adapt. Meanwhile, it is managing to keep itself in circulation. The new CoViD-19 variant—D614G—is situated within the protein forming the “spike” used by the virus to break into our cells. The spike is rather like a hacker who breaks through the cell’s firewall, finding a means to penetrate the cell membrane. The new variant must have emerged sometime after the initial Wuhan outbreak, most likely in Italy it is believed. It later emerged in 97% of samples around the world.
The question is whether this dominance, achieved through mutation, is intended to give the virus some advantage, or whether it is merely a random, chance occurrence. It is widely believed that viruses don’t really operate according to a grand plan. They mutate constantly, and while some changes will help a virus reproduce, some may hinder it. Other mutations are not really adaptive in nature, but merely neutral. They’re a “by-product of the virus replicating,” Dr. Lucy van Dorp of University College London explains, adhering to the view that they hitch-hike on the virus without changing its behavior.
It is thought that the mutation could have become very widespread just because it happened early in the outbreak and spread, a phenomenon known as the “founder effect.” This is what Dr. van Dorp and her team believe is the most likely explanation for the mutation becoming so common.
However, this view is now being called into question, as a growing number of virologists now believe, as Dr. Thushan de Silva of the University of Sheffield explains, there is enough data to say this version of the virus has a “selective advantage,” granting it an evolutionary edge over the earlier version.
Though there is still not enough evidence to say it’s more transmissible in people, he says, he is confident that the mutation is not neutral, but meant to grant it selective advantages. A laboratory-based study has revealed that the mutated virus was better at entering human cells than previous versions, say professors Hyeryun Choe and Michael Farzan, at Scripps University in Florida. Changes to the spike protein the virus uses to latch on to human cells has allowed it to “stick together better and function more efficiently.”
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Professor Farzan said the spike proteins of these viruses were different in ways that were “consistent with, but not proving, greater transmissibility.” At the New York Genome Center and New York University, Professor Neville Sanjana, an expert in the gene-editing technology known as CRISPR, made an even bolder assertion. His team edited a virus so that it contained an alteration in the spike protein and pitted it against a real SARS-CoV-2 virus from the early Wuhan outbreak. The two versions of the virus were unleashed in human tissue cells. The results, he believes, prove the mutated virus is more transmissible than the original version, at least in the experiment undertaken in a lab setting.
Dr. van Dorp, however, asserts that it is uncertain how representative it is of transmission in real patients. But Professor Farzan maintains that these “marked biological differences” were “substantial enough to tilt the evidence somewhat” in favor of the notion that the mutation was making the virus more pathogenic, meaning more transmissible.
What has happened outside the lab in the human population has provided researchers with some indirect evidence that the mutation has made the CoViD-19 virus more transmissible. Two studies have shown that patients infected with the mutated form of the virus have greater quantities of the virus showing up in their swab samples. This might suggest the virus had become more pathogenic, but not more virulent, since the evidence failed to show that the infected had become sicker or had longer hospital stays.
The fact that a virus is more transmissible does not mean that it is more pathogenic. In fact, the opposite often holds true. There is no evidence the CoViD-19 virus has mutated to make patients more ill. However, when it comes to transmissibility, viral load only indicates how well the virus spreads within a single person. It doesn’t necessarily account for how virulent it might be. The real litmus test, consisting of a controlled trial, had not yet been conducted to determine pathogenicity. Such a trial might involve, for example, infecting animals with either one or the other CoViD-19 variant to see which is more pathogenic.
One of the leaders of the study, Professor Bette Korber of Los Alamos National Laboratory in the U.S., said there was no consensus, but the claim that the mutation may have increased the viral load of those infected was “getting less controversial as more data accrues.”
The Mutation Is the Pandemic
When it comes to looking at the whole population, it is difficult to assess whether the virus is becoming more or less infectious. It is believed that its course has been drastically altered by interventions, including lockdowns. But Professor Korber says the fact the variant now appears to be dominant everywhere, including in China, indicates it may have developed mutations or adaptations to make it more pathogenic. Whenever the two versions circulated within the population at the same time, the new variant took over. In fact, the D614G variant is so dominant, it may have evolved into the form of the virus actually causing the pandemic. And it has been in that ascendant position for some time, perhaps even since the start of the pandemic in places like the UK and the east coast of the U.S.
Many scientists are of the opinion that most of the vaccines that have been in development are based on a different region of the spike, so the mutation does not appear to make the vaccines redundant. In addition, there is some evidence antibodies defend just as successfully against the new strain, which can offer protection against infection should an individual become infected, or be vaccinated against it, so scientists studying the different variants of the virus believe. But since the science of CoViD-19 is so fast-paced, scientists will have to remain vigilant in surveying and responding to further CoViD-19 adaptations or mutations. iii
Coronavirus Mutation Makes It More Pathogenic
A study involving more than 5,000 CoViD-19 patients in Houston has shown that the virus is cumulatively developing more genetic mutations, and the variation known as D614G may have made it more pathogenic. According to the paper published in the peer-reviewed journal mBIO, variant D614G, located in the spike protein, helps the virus penetrate the cell membrane to gain entry. It is the largest peer-reviewed study of SARS-CoV-2 genome sequences ever undertaken in one metropolitan region of the U.S.
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The number of virus strains present in each zip code in Houston during the second wave of CoVD-19 cases in summer 2020. Number of strains is represented by a spectrum of colors from blue (0 strains) to red (50 strains). Credit: Houston Methodist/University of Texas at Austin.
The paper shows the virus is mutating due to a combination of neutral drift—random genetic changes taking place within the virus itself—as well as immune system resistance, said Ilya Finkelstein, associate professor of molecular biosciences at The University of Texas and co-author of the study conducted by scientists at Houston Methodist Hospital, UT Austin, and elsewhere.
During the first wave of the pandemic, 71% of the CoViD-19 virus identified in Houston patients was found to be of the D614G strain. When the second wave hit Houston during the summer of 2020, the D614G variant had overtaken its predecessor, displaying a 99.9% prevalence, mirroring a worldwide trend. A study published in July of 2020, based on a survey of more than 28,000 genome sequences, found that it had only taken a month for variants carrying the D614G mutation to become the globally dominant SARS-CoV-2 version.
What scientists want to know is how did strains containing this mutation become the strongest in the survival of the fittest? One explanation is that the more recent variant had become more contagious. A study of more than 25,000 genome sequences in the U.K. found that viruses containing the mutation were more pathogenic, resulting in larger infection clusters. Most scientists are of the opinion that natural selection tends to favor more pathogenic strains of the virus emerging, but not all scientists are on board with that notion. Some have suggested that “founder’s effects” might be a more plausible explanation. If that is the case, then the D614G variant might have been more common in the first viruses to arrive in Europe and North America, gaining a foothold before other strains reached those shores.
It is believed that the spike protein continued to develop further mutations the significance of which could not be determined. The Houston Methodist-UT Austin team also conducted lab experiments to show that the D614G variant allows the spike to evade a neutralizing antibody meant to fight SARS-CoV-2 infections. This may allow that variant to more easily fly under the immune system’s radar.
While apparently more pathogenic, there is no evidence that the D614G strain is more virulent. According to Finkelstein, the group has not yet run into viruses that are able to evade first-generation vaccines and therapeutic antibody formulations. “The virus continues to mutate as it rips through the world,” Finkelstein said. “Real-time surveillance efforts like our study will ensure that global vaccines and therapeutics are always one step ahead.”
The scientists noted a total of 285 mutations across thousands of infections, though most don’t appear to amplify the virulence. There are ongoing studies being conducted on the third wave of CoViD-19 patients, analyzing how the virus is mutating in order to circumvent antibody defenses of the immune system. Each new infection offers a chance for the virus to develop more dangerous mutations. At some point, the genetic sequence will find the right combination of GTCA coding to hit the jackpot, resulting in a more pathogenic and virulent strain.
The UT Austin team tested different genetic variants of the virus’s spike protein in order to determine the protein’s stability and assess its efficiency in binding to receptors on host cells. Earlier in the year, McLellan and his team at UT Austin, in collaboration with researchers at the National Institute of Health, developed the first 3-D map of the CoViD-19 spike protein with the hope of developing an effective vaccine.
Researchers found that SARS-CoV-2 was introduced to the Houston locale from diverse geographic regions multiple times, including strains from Europe, Asia, South America, and other parts of the U.S. The variant seems to have dispersed widely within the community soon after CoViD-19 cases were reported in Houston.iv
While some studies have shown the SARS-CoV-2 virus increasing in pathogenicity, other studies are showing that it may be increasing in virulence as well. Researchers at Michigan State University developed a model machine learning application that suggests mutations of the SARS-CoV-2 genome may have increased in virulence. The model conducted a comparative analysis of the SARS-CoV-2 genotype in more than 20,000 viral genome samples. The researchers analyzed mutations of the spike protein, and found that five out of six known virus subtypes have been found to be more pathogenic.
As with any virus, many mutations are ultimately benign, posing little risk to infected patients, some actually reducing its pathogenicity surprisingly. However, some mutations are known to lead to a more pathogenic or virulent virus.
The team at Michigan State University studied and analyzed mutation patterns and locations, tracking the changes resulting in newer strains diverging from the official viral genome sample isolated in January of 2020.
“Knowledge about the infectivity of SARS-CoV-2 is a vital factor for preventive measurements against CoViD-19 and reopening the global economy,” the head researcher said. “A crucial question is what are the ramifications of these mutations to CoViD-19 transmission, diagnostics, prevention and treatment.”
It is believed that CoViD-19 infection occurs when the spike protein interacts with a human host cell receptor called angiotensin-converting enzyme 2 (ACE2). As it interacts with ACE2, scientists worry about the degree of “binding affinity” that occurs between the spike protein and host receptor during the initial stage of infection.
“Viral infectivity increases if the binding affinity strengthens,” the head researcher maintained. “Currently, more than 50 mutations have been found along with the binding interface on the spike proteins receptor-binding domain—RBD for short—which has 194 possible mutation sites.”
The team’s machine learning model, an advanced neural network, analyzed more than 8,000 protein interaction records to assess the impact of the SARS-CoV-2 spike protein binding affinity found in the most recent mutations. The results showed increased binding affinity in five of the six known subtypes, suggesting mutations may have led to increased infectivity, making the newer variants more pathogenic.
Concerned about the possibility of further mutation, the team applied their model to predicting potential future outcomes. “It’s extremely important to know whether future SARS-CoV-2 subtypes would pose an imminent danger to public health,” the head researcher said. “To this end, we have conducted a systematic screening of all possible 3,686 future mutations on 194 possible mutation sites along the RBD.”
The team’s model predicts that multiple residues on the receptor-binding structure—a component area of the RBD—have a greater chance of producing more infectious CoViD-19 mutations. The head researcher cautions that, though computer modeling can show consistencies with experimental findings, further studies are needed to fully understand impacts of mutations on CoViD-19 infectivity.
As part of their research, the team also predict that SARS-CoV-2 will prove to be slightly more infectious than the original SARS virus isolated in 2003. The head researcher said the study results match the findings of researchers at the Scripps Research Institute in Florida. This study examined spike protein mutations in a laboratory setting and found that the mutations are producing more pathogenic strains in more recent variants.v
Current observations suggest that SARS-CoV-2 causes severe symptoms mainly in elderly patients suffering from chronic disease. However, when two pairs of previously healthy young brothers from two families required mechanical ventilation at the intensive care unit in rapid succession, medical professionals at Radboud University Medical Center wondered if genetic factors might have played a role in crippling their immune systems. Research identified the gene TLR7 as a major player in the body’s immune response to SARS-CoV-2.
Amid the wave of CoViD-19 patients flooding Dutch hospitals in early 2020, two young brothers had to be mechanically ventilated in the ICU. One of them died, while the other recovered. The fact the disease had struck these healthy young brothers so severely was a rare occurrence, especially considering that, at that early stage of the pandemic, the elderly had seemed more susceptible and vulnerable to the virus. This prompted an attentive physician from the department of clinical genetics to take a closer look. She and her team tried to determine what made the two young brothers so susceptible.
Soon after, doctors and researchers at Radboudumc encountered another pair of brothers who had also been ravaged by the disease. Again, both brothers were under 35, and like the former pair, they had also been placed on ventilators. Hoischen explains:
Then the question of the role of genetics became even more obvious. We also investigated the genetic code of these two brothers, again via the ‘rapid-clinical exome’ method. This time we saw no deletion, no loss of letters, but a single spelling mistake of one DNA-letter of the TRL7 gene. The effect on the gene is the same, however, because these brothers also do not make sufficient functional TLR7 protein. Suddenly we had four young people with a defect in the same gene, all of whom had fallen seriously ill from the SARS-CoV-2 virus.
Essential Role in the Defense
Van der Made and colleagues have investigated the consequences of improper functioning of the TLR7 receptor, a problem for which he offers the following explanation:
Once activated, TLR7 triggers the production of so-called interferons, signaling proteins that are essential in the defense against virus infections,” says van der Made. “This immune response is perhaps all the more important in the fight against the SARS-CoV-2 virus, because we know from the literature that the virus has tricks to reduce the production of interferons by immune cells. When we mimic an infection with the coronavirus, we see that immune cells of the patients without properly functioning TLR7 hardly respond, and that minimal amounts of interferons are produced. These tests make it clear that the virus appears to have free rein in people without properly functioning TLR7 because it [the virus] is not recognized by the immune system.
Due to the serious illness of four brothers in two families, so serious that it cost one of the young men his life, we have discovered this condition. It seems to be a very specific abnormality, an immunodeficiency, which is mainly related to this coronavirus. None of the four men have previously suffered from immune-related diseases. It is the first time that we can connect a clinical phenomenon so strongly with TLR7.
“This discovery not only provides us with more insight into the fundamental workings of the immune system, but it may also have important consequences for the treatment of severely ill CoViD-19 patients,” says Frank van de Veerdonk, immunologist and infectiologist. “The substance interferon can be given as a therapy. It is currently being investigated whether administering interferon in CoViD-19 can indeed help.”
This confirms that genetic defects in some genomes do make certain patients more vulnerable to the ravages of the disease. There are a variety of reasons for this, but it can generally be deduced that the immune response may be less efficient due to the genetic makeup of certain patients. This discourse will delve into several examples of this. Sadly, like many diseases, there seems to be a separating of the wheat from the chaff, a kind of natural selection process that is taking out those with a less vigorous and robust constitution, or less efficient immune system, so that in the end, only the strongest appear immune or more likely to survive.vi
There is an additional perhaps more worrying aspect of this problem in that the disease seems to be chewing at the bottom end of the evolutionary tree, such that those with a high ratio of Neanderthal and Denisovan genetics in their genome are more vulnerable to the disease. This suggests the possibility that viruses may play an inherent role in natural selection and deselection, in the sense that whole genomic profiles could be removed from the tree of life known as the human gene pool.
It would appear from the foregoing that genetic variability in the human immune system may affect susceptibility to the disease, as well as severity of infection for those who contract SARS-CoV-2. Research into this question has been published in the Journal of Virology, a publication of the American Society for Microbiology.
The study into individual genetic variation may account for the effectiveness of various immune responses. It has been discovered that certain immune system genes called human leukocyte antigen genes, involved in recognizing pathogens, tend to vary in terms of their effectiveness from person to person. Genetic variations in individuals appears to have an effect on how well the immune system recognizes a given pathogen. Poor recognition of SARS-CoV-2, where the virus fails to show up on the body’s immune system radar, could make a person more vulnerable to attack by the virus.
“In particular, understanding how variation in HLA [a component of the immune system containing multiple genes] may affect the course of CoViD-19 could help identify individuals at higher risk from the disease,” the authors of the study claim. The authors showed that individual HLA, haplotype, and full genotype variability most likely have a bearing on the individual patient’s capacity to fight off SARS-CoV-2 infection. The authors also note that certain alleles could be associated with more severe infection. To understand what is meant by “alleles,” picture red and white flowers and the combinations of colors they produce generationally. At times, a pink hybrid, or some other color variant, will skip a generation or two and show up in a subsequent generation. The same anomalies determine variations in the genetic disposition of humans, and one’s allele can have an effect on how vigorously one’s immune system is able to fight off SARS CoV-2. “This is the first study to report global distributions of HLA types and haplotypes with potential epidemiological ramifications in the setting of the current pandemic,” write the authors, from Oregon Health & Science University, Portland, and the Portland VA Research Foundation.
The authors show that individual HLA haplotype, and full genotype variability probably have a strong impact on the patient’s capacity to respond to SARS-CoV-2 infection, and note that certain alleles in particular could contribute to more severe infection, as had previously been shown with SARS-CoV.
“HLA typing can be fast and inexpensive,” the authors write. “Pairing HLA typing with COVID-19 testing where feasible could improve assessment of viral severity in the population. Following the development of a vaccine against SARS-CoV-2, the virus that causes COVID-19, individuals with high-risk HLA types could be prioritized for vaccination.”
Once again there is evidence that genetics plays a role in who might have greater susceptibility to the ravages of CoViD-19. The immune response of some patients has been shown to be more efficient than others, and in many cases, a common denominator has been found in certain features of the genomes of those affected. This is an important discovery, and may point to the role viruses play in evolution, as there are indications that patients who suffer from low IQ levels, obesity, diabetes, and other comorbidity factors, turn out to be more susceptible to infection, have weaker immune responses, and have less chance of survival and recovery than people who are genetically and medically sounder. This could point to two possibilities: either God is a eugenicist or some men in lab coats working in some bioweapon facility, engineered a gain-of-function bioweapon to take out the less constitutionally fit and genetically sound.vii
In the competition for survival between Neanderthals and Homo sapiens, were we Homo sapiens the fittest and therefore the ones to survive, leaving our Neanderthal cousins in the dust, or is it more accurate to suggest that we interbred, so that, to an extent, they became us, and we, them? And what of the impossibly singular Mitochondrial Eve, her contemporary Y-chromosome Adam, and the African origin hypothesis? Are these valid theories or simply convenient fictions devised by paleogeneticists to grant their largely arbitrary haplotype classifications greater credence, and their complementary evolutionary trees greater validity?
Svante Pääbo, director of the genetics department at the Max Planck Institute, certainly believes that Homo sapiens Neanderthalensis, or just Homo Neanderthalensis, if you prefer, is extinct. Pääbo, the son of 1982 Noble laureate Sune Bergström, has made a career out of studying Neanderthal bones, finding every gene sequence to be distinctly Neanderthal in nature. In 1997, Pääbo successfully sequenced mitochondrial DNA from a specimen found in the Feldhofer grotto in the Neander valley.
Amazing as it sounds, it is possible that the coronavirus may play a role in settling the issue of what became of our Neanderthal cousins, and whether we blended our genome with theirs or not. As discovered by Pääbo and his colleague, Hugo Zeberg, the major genetic risk factor for developing severe CoViD-19 infection is inherited from Neanderthals. The team found that severe CoViD-19 infection is associated with specific genetic variants in six genes within a 50K-base-pair-long region of chromosome 3 that shows direct Neanderthal descent. Similar investigations have also identified a protective Neanderthal haplotype found on chromosome (chr) 12 that reduces the risk of contracting severe CoViD-19, and a protective region on chromosome 9 that is associated with the ABO blood groups.
Pääbo and Zeberg recently reported that another exclusively Neanderthal variant found in the promoter region of the DPP4 gene, at chr2q24.2, is the Achille’s heel in terms of CoViD-19 susceptibility. DPP4 is a widely expressed extracellular dipeptide peptidase tied to immune function and glucose metabolism. As it happens, DPP4 is also the receptor gene for the MERS coronavirus. This common denominator between the MERS virus and the SARS-CoV-2 coronavirus provides a clue to where the weak point in the genetic chain is that causes some to be more susceptible to infection than others.
Although other researchers have insisted DPP4 is not a SARS-CoV-2 receptor, inhibitors of DPP4 already used clinically to treat diabetes appear to have effects on CoViD-19 patients. Genetic research into SARS has revealed that a handful of immune-associated gene variants, including IFNAR2 and TYK2, happen to have an influence on CoViD-19 susceptibility. It happens that this study also identified DDP9, a sister gene of DD4 found at chr19p13.3, as a key mediator of inflammatory lung injury. DPP9 shows a similar serine protease activity to DPP4, but differs in not being membrane-bound.
The DPP4 gene is located fairly close to a long-defunct remnant centromere found nearby in the chr2q21.3–q22.1 region. There is also a vestigial telomere found in the q13 band. It begs the question as to what purpose these structures actually serve. A plausible answer is that fusion of two small ape chromosomes has occurred to produce the human chr2. Do Neandertals have a fused chr2? It turns out that they actually do.
Not only that, but they seem to have the same version of the speech gene, FOXP2, which Pääbo identified in 2002. Human FOXP2, which differs from the chimp version in two key places, was famously mutated in the “KE” family from Britain, who all happened to express a specific disability in their use of consonants. In the more recent CoViD-19 risk factor study, Pääbo searched for single nucleotide polymorphisms using data from the 1000 Genomes Project, then checked with the CoViD-19 Host Genetics Initiative to see if Neanderthal haplotypes for DDP4 had any association with disease severity.
The problem with this line of inquiry is that we don’t have that much sequence data to tell us what makes a Neanderthal by definition what it is. There are only a few good genomes available from skeletal remains 120,000 years old and 50,000 years old, respectively, all of which come from Europe and southern Siberia.
If it has done anything, the CoViD-19 epidemic has exposed the fact that blind medicine is no longer satisfactory. Blind medicine refers to analysis done in the absence of personal patient sequence data. When genomics data is given with respect to a reference sequence, problems frequently arise. This is due to the fact that there is no such thing as a reference sequence, as it too is completely arbitrary. Updates and improvements are occasionally made to various reference sequences, but no true reference sequence will ever be available.
In contrast to the MERS DPP4 receptor, no ACE2 receptor variants have been isolated as a risk factor for severe CoViD-19 infection. However, many of the other genes associated with SARS-CoV-2 infection and its life cycle have been discovered. For example, four variants—rs464397, rs469390, rs2070788 and rs383510—robustly affect expression of the TMPRSS2 serine protease in lung tissue. TMPRSS2-unregulating variants tend to be found at higher frequencies in European and American populations than in their Asian counterparts.
Perhaps of more immediate concern, now that vaccines are becoming available, is who among its recipients, is the vaccine likely to prove beneficial or harmful to. The latter prospect is usually explained as antibody-dependent enhancement (ADE). As for diseases like Dengue fever or respiratory syncytial virus, ADE is taken very seriously, though ADE is usually dismissed out of hand in discussions of CoViD-19. However, recent research now suggests that ADE is very much a problem in the case of CoViD-19 patients.
In particular, researchers have found that some anti-spike monoclonal antibodies from CoViD-19 patients—particularly those meant to oppose the N-terminal-domain (NTD) of the spike—dramatically enhanced the binding capacity to ACE2, thereby enhancing SARS-CoV-2 infectivity. Mutational analysis was able to pinpoint a specific surface region of the NTD, revealing that those patients taking part in the study had antibodies against this infectivity-enhancing site. As information about spike sequence mutations and ADE risk factors were updated much faster than vaccine development times, it is important for the public to get information about the mRNA vaccines currently on offer. Namely, what exact spike sequences is the vaccine meant to replicate in order to generate an antibody response?
There are serious concerns among some medical professionals and epidemiologists that the mRNA vaccines could produce autoimmune disease in patients. The belief is that, by reprogramming cells to produce similar spike proteins to those of the virus, it is hoped it will program an antibody response toward the spike proteins in the CoViD-19 virus itself. The problem is that the spike proteins produced by the cell by means of the transcription and translation instructions received from the RNA, as programmed by the mRNA vaccine, will cause these spike proteins to proliferate and embed themselves in blood vessel walls and in the healthy cell tissue of the heart, lungs and other organs, prompting the antibodies to mobilize and go on the offensive to attack such sites, causing them to attack the body’s organs, cell tissue and even the protective lining of blood vessels, resulting in blood clots, hemorrhaging, internal bleeding, and cardio-pulmonary disease.
Recent reports of new proliferations of spike mutants have raised further questions. How could the vaccine-evading N501Y variant in the receptor binding domain or the double-NTD-deletion variants constitute possible game-changers in the fight against CoViD-19? Or how does the new D614G spike variant, alleged to confer more efficient replication, affect the pathogenicity of the virus? These are serious questions that must be addressed.viii
Many scientists now believe that genes that some people have inherited from their Neanderthal ancestors may significantly increase their likelihood of suffering severe forms of SARS-CoV-2 infection. As has been argued, the disease seems to be ravaging the lower end of the evolutionary tree, chewing on haplotypes with a high Denisovan or Neanderthal genomic profile. Such haplotypes have been found to be quite prevalent in Far East Asia and South Asia, as well as among Brazilians, and aboriginal populations in the Americas. Once this is considered, it raises provocative questions about the true purpose of the caste system in the Hindu religious culture of India. There is no doubt that the caste system of India was meant to enforce a code of racial hygiene intended to protect the Aryan population base of the higher Brahman caste. Is it possible that Hindu gurus and adepts recognized that racial hygiene was necessary in order to protect the constitutional health of the Brahmin caste by preventing their haplotype from being tainted by constitutionally less vigorous genomes?
A study by European scientists published in the journal Nature examined a cluster of genes that have been linked to a higher risk of hospitalization and respiratory failure in patients infected by CoViD-19.
Zeberg and Paabo, in particular, have concluded from their research that the genes in question belong to a genetic haplotype group, which likely came from Neanderthals. The haplotype is present in about 16% of the European population and approximately 50% of South Asians, while in Africa and East Asia it is virtually non-existent.
It has been established that modern humans and Neanderthals have interbred at various points in history, resulting in an exchange of genes than can still be found in certain human populations today. The genes are one of several risk factors for CoViD-19 patients, including age, sex, and pre-existing conditions like obesity, diabetes, and heart problems.
Zeberg and Paabo noted that the prevalence of the particular Neanderthal gene group is highest in people from Bangladesh, where 63% are estimated to carry a copy of the haplotype. And this has led this author to an interesting parallel between the susceptibility of Bangladeshis to CoViD-19 infection and the infection rate found in a segment of the South Asian immigrant population found in the Toronto satellite town of Brampton, which has experienced a high incident rate of CoViD-19 infection, and which just happens to have a high ratio of immigrants from Bangladesh.
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These genetic variants are almost completely absent in Africa and occur in the highest frequency in Bangladesh. Credit: Professor Svante Pääbo and Professor Hugo Zeberg/Nature
Zeberg and Paabo cited studies from the UK, which show that people of Bangladeshi descent have roughly two times greater chance of dying from CoViD-19 as the general population. “It is striking that the genetic heritage from the Neanderthals has such tragic consequences during the current pandemic,” Paabo recently observed. “Why this is must now be investigated as quickly as possible.”
However, despite Paabo’s call to action, Andre Franke, director of the Institute of Clinical Molecular Biology at the University of Kiel, Germany, said the findings have no immediate effect on the approach medical professionals will adopt in treating CoViD-19. Franke did suggest, however, that one interesting question arising from the study is why this particular haploytpe—unlike most Neanderthal genes—has managed to survive until now. “Perhaps it’s good for a very active immune system if one doesn’t have other risk factors,” he observed.ix
In concurrence with the findings of Zeberg and Paabo, it has been discovered that an area in the north corner of Brampton, a satellite city of Toronto, Ontario, Canada, has a shockingly high 19% CoViD-19 positive test rate, and holds the lead in the Greater Toronto urban zones that are witnessing alarming numbers of positive cases. Peel Region is showing a positivity rate of 9.8%—the highest in the GTA—while neighborhoods in western Toronto, Scarborough, and southern York Region are also reporting high rates. In one area of Brampton north of Queen St. E. and east of Airport Rd., one in five people have tested positive for the virus, which is five times higher than the average for the whole province of Ontario. The Brampton neighborhood with the highest positivity rate includes a number of small geographical areas defined by Statistics Canada. Of these zones, nine had infection rates of 200 per 100,000 people in November 2020, according to Peel Region Public Health, five times the infection rate required to move an area into the province’s ‘red’ or ‘control’ zone, which would require stringent lockdown measures.
It also happens that this area has Peel Region’s highest proportion of large households, with 49% of homes occupied by five or more people. Peel shows a house occupancy rate higher than Toronto or Ottawa, according to medical officer of health, Dr. Lawrence Loh. Additionally, household contacts have accounted for 40% of the CoViD-19 cases in most recent data collection efforts. As a result, the government implemented plans to build a facility in the area to house people who cannot properly self-isolate in their own homes. This area of Brampton is also densely populated with essential workers. One community of about 2,360 residents has Peel’s highest proportion of people working in the manufacturing sector, with 22% of residents drawing their living from this industry.
Just north of this area is another census zone with Peel’s highest level of retail workers at 16%, and with the lowest level of education, where 60% of residents possess no post-secondary school education. The community of 7,000 reported 66 cases of CoViD-19 in the first three weeks of November 2020. Its infection rate at the time was recorded as 285 cases per 100,000. These are racialized neighborhoods, where there are significant levels of poverty and overcrowding. There are also a significant number of essential workers who are low salary earners and can’t afford to stay home, according to Colin Furness, an infection control epidemiologist at the University of Toronto.
While the government is addressing the health concerns in the area responsibly, with mobile testing and isolation measures, the rising number of cases is still cause for concern. Should people test positive, they stay in hotel rooms, where they receive free food and care. There are even initiatives to provide financial incentives for people to come in and get tested in a move to stave off the spread of infection.x
What is not mentioned by any of the epidemiologists or specialists studying the problem is the genetic factor. Some studies indicate that the virus is attacking people with certain genetic profiles. Low IQ has come up as a factor in some studies. However, in this particular case, the affected area of Brampton with the highest incidence of CoViD-19 infection has a high percentage of Bangladeshis, who just happen to have a high ratio of Neanderthal genetics in their genome. Some will find such information politically incorrect to share, but the point of transparency in all issues is that “the truth shall set us free.” Concealing or covering up the truth invariably leads to more problems than it solves. Unless we can openly discuss these issues and all related ramifications, we are not going to find the solutions to stop the spread of such diseases. We have to cure ourselves of the phobias, cultural stigmas, and biases first before we can succeed in defeating this and other contagious diseases. What is most medieval in our society is the taboos that prevent the truth from being shared and openly discussed, and there is really no place for that kind of adolescent behavior if we hope to build a more progressive society in the 21st century, unless of course the majority prefer to be regressive, in which case, God help us.
Census data presents clues for why the positivity rates have such a high spike in this community, which just happens to have a high concentration of visible minorities, especially South Asians. Socioeconomic data shows that South Asians have been disproportionately hard hit by CoViD-19 in Peel Region, accounting for 45% of cases while comprising only 32% of the region’s population.
A recent genetic association study has identified a gene cluster on chromosome 3 as a risk factor in respiratory failure following infection by the severe acute respiratory syndrome SARS-CoV-2. A separate study—CoViD-19 Host Genetics Initiative—comprising 3,199 hospitalized patients with CoViD-19 and control individuals, showed that this cluster is the major genetic risk factor for those suffering from severe symptoms related to SARS-CoV-2 infection and hospitalization. The risk is conferred by a genomic segment of around 50 kilobases in size inherited from Neanderthals and is carried by around 50% of people from South Asia and around 16% of Europeans.
The CoViD-19 pandemic has caused a considerable degree of infection and mortality, with some statistical data suggesting it has resulted in the death of over a million people worldwide by early 2021. Although it is hard to trust the accuracy of such statistics, since they have been greatly exaggerated by the fact that many families of deceased patients are encouraged to lie, attributing their relative’s death to CoViD-19 as opposed to the true cause of death, since both the hospital and the patient’s family receive money payouts whenever CoViD is identified as the cause of illness and death.
The clinical manifestations of the disease caused by the virus, SARS-CoV-2, vary widely in severity, ranging from an absence of symptoms to mild symptoms to rapid progression to respiratory failure. Early in the ‘pandemic,’ it became clear that old age was a major risk factor. Another increased risk factor was being of the male sex. In addition, some co-morbidity factors such as diabetes or obesity proved a danger and quite often increased the risk of fatality from CoViD-19 infection. These risk factors, however, do not fully explain why some people have a complete absence of symptoms or relatively mild symptoms, while others experience severe symptoms. It has therefore been postulated that genetic risk factors may play a role in disease progression. A previous study identified two genomic regions associated with severe CoViD-19 infection: one region on chromosome 3 containing six genes, and one region on chromosome 9 that determines ABO blood groups. Recently, a dataset was released by the CoViD-19 Host Genetics Initiative, in which a region on chromosome 3 was identified as the only region found to bear a significant relationship to severe CoViD-19 at the genome-wide level. The risk variant in this region has been blamed for an odds ratio requiring hospitalization of 1.6 (95% confidence interval, 1.42–1.79).
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Fig. 1: Genetic variants associated with severe CoViD-19
In figure 1 above, a, shows a Manhattan plot of a genome-wide association study of 3,199 hospitalized patients with CoViD-19 and 897,488 population controls. The dash line indicates genome-wide significance (P = 5 × 10−8). Data were modified from the CoViD-19 Host Genetics Initiative2. Figure b shows a linkage disequilibrium between the index risk variant (rs35044562) and genetic variants in the 1000 Genomes Project. Red circles indicate genetic variants for which the alleles are correlated to the risk variant (r2 > 0.1), where risk alleles just happen to match the Vindija 33.19 Neanderthal genome. The core Neanderthal haplotype (r2 > 0.98) is indicated by a black bar. Some individuals carry longer Neanderthal-like haplotypes. The location of the genes in the region are indicated below using standard gene symbols. The x axis shows hg19 coordinates.
The genetic variants found to have the strongest connection with severe CoViD-19 on chromosome 3 (45,859,651–45,909,024 (hg19)) are all in high linkage disequilibrium (LD)—which means they are all strongly associated with each other in the population (r2 > 0.98)—and span 49.4 thousand bases (kb). This core haplotype has been found to express a weaker linkage disequilibrium with longer haplotypes of up to 333.8 kb (r2 > 0.32). Some long haplotypes have entered the genome of modern humans from Neanderthals or Denisovans, extinct hominins that contributed genetic variants to the ancestors of present-day humans around 40,000–60,000 years ago. This prompted the authors of the study to investigate and verify whether the haplotype did indeed come from Neanderthals or Denisovans.
The index variants of the two studies are in high linkage disequilibrium (r2 > 0.98) in non-African populations. We found that the risk alleles of both of these variants are present in a homozygous form in the genome of the Vindija 33.19 Neanderthal, a Neanderthal found to be approximately 50,000 years old from Croatia in southern Europe. Of the 13 single nucleotides polymorphisms constituting the core haplotype, 11 occur in a homozygous form in the Vindija 33.19 Neanderthal. Three of these variants occur in the Altai and Chagyrskaya 8 Neanderthals, both of whom come from the Altai Mountains in southern Siberia and are estimated to be 120,000 and 60,000 years old, respectively, whereas none of the variants occur in the Denisovan genome. In the 333.8-kb haplotype, the alleles associated with risk of acquiring severe CoViD-19 similarly match alleles in the genome of the Vindija 33.19 Neanderthal. It has therefore been found that the risk haplotype is similar to the corresponding genomic region in the Neanderthal from Croatia and less similar to its counterpart from Siberia.
The investigation then led to an examination of whether the core 49.4-kb haplotype might be inherited by both Neanderthals and present-day people from the common ancestors of the two groups that lived about 0.5 million years ago. The longer a present-day human haplotype has been shared with Neanderthals the less it is that it orginated from a common ancestor, because recombination in each generation would tend to break up haplotypes into smaller segments. Assuming a generational time of 29 years, with the local recombination rate (0.53 cM per Mb), a split between Neanderthals and modern humans is thought to have occurred 550,000 years ago, while interbreeding between the two groups is found to have occurred around 50,000 years ago. Using a published equation, the authors of the study have chosen to exclude the possibility that the Neanderthal-like haplotype has been derived from the common ancestor (P = 0.0009). As for the 333.8-kb-long Neanderthal-like haplotype, the probability of an origin from the common ancestral population is even lower (P = 1.6 × 10−26). The risk haplotype contributing to CoViD-19 susceptibility thus entered the modern human population from Neanderthals. This finding concurs with several previous studies, which have identified gene flow from Neanderthals in particular chromosomal regions. The close relationship of the risk haplotype to the Vindija 33.19 Neanderthal is compatible with this Neanderthal being closer to the majority of the Neanderthals who contributed DNA to present-day humans than the other two Neanderthals.
A Neanderthal haplotype found in the genomes of present-day humans is expected to express greater similarity to a Neanderthal genome than to other haplotypes in the current human population. In order to investigate the relationship of the 49.4-kb haplotype to Neanderthal and other human haplotypes, the authors of the study analyzed all 5,008 haplotypes in the 1000 Genomes Project for this genomic region. They included all relevant positions found in the Neanderthal genomes and excluded variants found on only one chromosome and haplotypes seen only once in the 1000 Genomes Project data. The results of the study revealed that there were 253 present-day haplotypes containing 450 variable positions. There is a related phylogeny in the haplotypes that were found more than 10 times. The authors of the study found that all risk haplotypes associated with severe CoViD-19 form a species’ clade featuring the three high-coverage Neanderthal genomes. This clade is found to be most closely related to the Vindija 33.19 Neanderthal.
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Fig. 2: Phylogeny relating the DNA sequences that covers the core Neanderthal haplotype in individuals from the 1000 Genomes Project and Neanderthals
The colored area in the chart above shows the haplotypes that carry the risk allele at rs35044562, which just happen to be the risk haplotypes for severe CoViD-19. Arabic numbers indicate bootstrap support (100 replicates). The phylogeny is rooted with the inferred ancestral sequence of present-day humans. The three Neanderthal genomes carry no heterozygous positions in this region. The scale bar shows the number of substitutions per nucleotide position.
Among the individuals in the 1000 Genomes Project, the Neanderthal-derived haplotypes are almost completely absent from Africa, which is consistent with the theory that gene flow from Neanderthals into African populations was limited and probably indirectly infused from western migratory population inflows from the Altai Mountains region. The Neanderthal core haplotype occurs in the South Asian population with an allele frequency of 30%, an allele frequency of 8% in the European population, an allele frequency of 4% among admixed Americans, and with lower allele frequency levels found in East Asia. In terms of carrier frequencies, 50% of people in South Asia were found to carry at least one copy of the risk haplotype, whereas 16% of Europeans and 9% of admixed Americans were found to carry at least one copy of the risk haplotype. The highest carrier frequency occurs in Bangladesh, where more than half the population (63%) carries at least one copy of the Neanderthal risk haplotype, and where 13% is found to be homozygous for the haplotype. The Neanderthal haplotype can therefore be considered a substantial risk factor in CoViD-19 susceptibility, in addition to other probability factors, including old age. Immigrants of Bangledeshi origin living in the UK have a two times higher risk of mortality from CoViD-19 infection than the general population (hazard ratio of 2.0, 95% confidence interval, 1.7–2.4).
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Fig. 3: Geographical distribution of the Neanderthal core haplotype that confers risk of severe CoViD-19 infection
The pie charts show the minor allele frequency at rs35044562. Frequency data were obtained from the 1000 Genomes Project. Map source data were obtained from OpenStreetMap.
It is notable that the Neanderthal risk haplotype occurs at a frequency of 30% in South Asia, whereas it is almost absent in East Asia. This disparity in allele frequencies between South and East Asia is unusual (P = 0.006) and indicates that it may have been affected by selection in the past. Indeed, previous studies have suggested that the Neanderthal haplotype has been positively selected in Bangladesh. One possible explanation for this could be that it may have afforded protection against other pathogens. It is also possible that the haplotype has decreased in frequency in East Asia due to negative selection, perhaps because of coronaviruses or other pathogens eliminating whole pockets of population. In any case, the CoViD-19 risk haplotype on chromosome 3 is similar to some other Neanderthal and Denisovan genetic variants that have achieved high rates of incidents in some populations. This is owing to positive selection or drift, but it is now under negative selection as a result of the CoViD-19 pandemic.
It is currently not known what feature in the Neanderthal-derived region confers risk of severe CoViD-19 infection, and whether the effects of such features are specific to SARS-CoV-2, other coronaviruses, or other pathogens. Once the relevant genetic feature is identified, it may be possible to speculate about the susceptibility of Neanderthals to relevant pathogens. However, with respect to the current pandemic, it is clear that those with strong Neanderthal genetic profiles appear to have a quite tragic Achilles’s heel.xi
Breeding Between Homo sapiens and Neanderthals
Based on the gene sequences found in the genome of modern humans, it is fairly conclusive that our ancestors had encounters with Neanderthals, and that sexual congress it thought to have occurred in some cases. This is thought to have taken place between 37,000-42,000 years ago.
In February 2002, two explorers made an extraordinary discovery in an underground cave system in the southwestern Carpathian Mountains, near the Romanian town of Anina. Gaining access to this cave complex was no easy matter. First, the explorers had to wade in an underground river up to their necks for 200m (656ft), a haunting experience that must have made them wonder if they has traversing the River Styx and in the midst of crossing over to the other side. Then came a scuba dive for 30m (98ft) along an underwater passage, followed by a 300-metre (984ft) ascent up to the “mouse hole,” an opening through which they entered a newly discovered chamber.
Inside the Peştera cu Oase (Cave with Bones), they found thousands of mammalian bones. Over its long history, the cave was thought to have been inhabited mainly by male cave bears—extinct relatives of the modern brown bear. Among these bones, they discovered a human jawbone, which radiocarbon dating revealed to be from one of the oldest known early hominids in Europe.
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The site of the discovery in the Southern Carpathian Mountains (Credit: NPL/Alamy)
Scientists have noted that, while the jawbone was unmistakeably modern in appearance, it also contained some unusual, Neanderthal-like features, a conjecture that was later confirmed. When scientists analyzed DNA from the jawbone in 2015, they found that, not only was the individual male, but was likely to have been 6-9% Neanderthal. This is the highest concentration ever found in the skeletal remains of an early modern human, and around three times the amount found in present-day Europeans and Asians, whose genetic makeup is estimated to be about 1-3% Neanderthal.
Because the genome contained large stretches of uninterrupted Neanderthal sequences, the authors of the study calculated that the jawbone’s owner is likely to have had a Neanderthal ancestor as recently as four to six generations back, equivalent to a great-great-great-great grandparent.
In addition to the jawbone, the team found skull fragments from another individual at Peştera cu Oase, who possessed a similar mixture of features. Scientists have not yet been able to extract DNA from these remains, but like the owner of the jawbone, it is thought that this individual may have had a very recent Neanderthal forebear.
Since then, there has been a growing body of evidence that sex between early modern humans and Neanderthals was a relatively common occurrence. Hidden in the genomes of present-day human populations, there are tell-tale signs that sexual liaisons between the two hominid populations happened frequently across a wide geographical area. To this day, there are people carrying genetic material from at least two different populations of Neanderthals, which one analysis suggests interbred with humans on several occasions in both Asia and Europe.
In fact, Neanderthal DNA can be found in every human being living today, including people of African descent, whose ancestors are believed to have had no direct contact with Neanderthals. In fact, in this case, the transfer of Neanderthal genetics is thought to have happened through indirect contact resulting from waves of migrations from the Altai Mountain region. In 2016, scientists discovered that Neanderthals from the Altai mountains in Siberia may have shared 1-7% of their genetics with the ancestors of modern humans, who lived roughly 100,000 years ago.
Male or Female Neanderthals
It’s impossible to say for certain whether it was mostly female Neanderthals scoring with early modern human males, or the other way around, but there is some evidence of sex occurring between the two species.
In 2008, archaeologists discovered a broken finger bone and single molar tooth in the Denisova Cave in Russia’s Altai Mountains, providing evidence for a brand-new subspecies of humans. For years, the “Denisovans” were known only from the handful of samples unearthed at this site, along with their DNA, from which scientists discovered that their legacy continues to this day in the genomes of people of East Asian and Melanesian descent.
Denisovans were a lot more closely related to Neanderthals than present-day humans; the two subspecies may have had ranges that overlapped in Asia for hundreds of thousands of years. This became particularly apparent in 2018, with the discovery of a bone fragment belonging to a young girl who scientists nicknamed ‘Denny’, who had a Neanderthal mother and Denisovan father.
Consequently, it would make sense if the male sex chromosomes of Neanderthals resembled those of Denisovans. But when scientists sequenced the DNA from three Neanderthals, who lived 38,000-53,000 years ago, they were surprised to discover that their Y chromosomes had more in common with those of present-day humans.
The researchers say this is evidence of “strong gene flow” between Neanderthals and early modern humans, suggesting that interbreeding between the species had become so common that, as Neanderthal numbers dropped to the point of extinction, their Y chromosomes may have been completely subsumed by ours, suggesting a form of extinction resulting from genetic assimilation. This suggests that a substantial number of ancestral human men were having sex with female Neanderthals.
But the story doesn’t end there. Other research has shown that almost exactly the same fate befell Neanderthal mitochondria—organelles found within cells that help turn sugars into useable energy. These are exclusively passed down from mothers to their children, so when early modern human mitochondria were found in Neanderthal remains in 2017, it hinted that our ancestors were also having sex with male Neanderthals. This time, the interbreeding is likely to have happened between 270,000 and 100,000 years ago, when humans were mostly confined to Africa.
What STD Infection Patterns Among Ancient Ancestors Reveal
A few years ago, Ville Pimenoff was studying the sexually transmitted infection human papillomavirus (HPV) when he discovered that there are more than 100 different strains believed to be responsible for 99.7% of cervical cancers worldwide. Of these, one of the deadliest is HPV-16, which lingers in the body for years, quietly corrupting the cells it infects.
But there is a clear divide globally concerning where certain variants of this virus are found. Across the majority of the planet, one tends to run across type A, while in sub-Saharan Africa, most people are infected with types B and C. Intriguingly, the pattern exactly matches the distribution of Neanderthal DNA worldwide. The people of sub-Saharan Africa, for instance, not only carry unusual strains of HPV, but also carry very little of the Neanderthal haplotype in their genome. Infection patterns of HPV may seem irrelevant to our coronavirus discussion, but this not so. There is a pretty straightforward corollary, as the infection patterns and susceptibility to HPV can be related to CoViD-19 infection patterns among certain haplotypes.
Pimenoff used the genetic diversity found in type A today to determine that it must have emerged roughly 60,000 to 120,000 years ago. This makes it much younger than the other kinds of HPV-16. Quite significantly, this just happens to be around the time that early modern humans emerged from Africa, and came into contact with Neanderthals. Although it is hard to prove definitively, Pimenoff believes the two hominid species immediately began swapping sexually transmitted diseases, and the split in the variants of HPV-16 reflects the fact that we acquired type A from their antecedents.
“I tested it thousands of times using computational techniques, and the result was always the same—that this is the most plausible scenario,” says Pimenoff. Based on HPV infection patterns found today, he suspects that the virus wasn’t just transferred once to the human population, but multiple times. “It is very unlikely that it just happened once, because then it would be more probable that transmission would not survive further,” says Pimenoff. “These sexual encounters must have been rather typical in Eurasia, in areas where both human populations were present.”
Intriguingly, Pimenoff also believes the acquisition of type A from Neanderthals explains why it is so cancerous in humans, since we became infected more recently than Neanderthals and our immune systems have not yet developed the adaptation feature needed to expurgate it.
When one considered the effect of disease transfer between populations, the separations of the castes in India—a practice introduced by Aryan invaders—may have occurred in response to the sudden appearance of diseases never before seen in their population, causing them to deduce that STDs and other diseases had occurred because some of their ranks had bred with the Dravidian native population. This may have caused the Aryans to infer from this that the Dravidians were inferior and had tainted their genetics through crossbreeding, causing them to fall ill, which they may have seen as a curse or even judgment of their god. This may have led them to institute the caste system in order to genetically segregate their population from others considered inferior and even accursed.
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Neanderthals (right) had projecting faces, low foreheads with pronounced browridges, wide cheekbones and weak chins compared to Homo sapiens (Credit: Sabena Jane Blackbird/Alamy)
In fact, sex with Neanderthals might have left Homo sapiens with an unwanted inheritance consisting of STDs, including an ancient relative of HIV. However, it seems we gave back as good as we got, as there is evidence that our Neanderthal cousins also inherited some STDs from us, including herpes.
Though it might seem crass to wonder what Neanderthal penises and vaginas were like, the fact is that an animal’s sexual organs can reveal a surprising amount about its lifestyles, mating practices, and even its evolutionary history. In fact, scientists recently discovered that the genetic code for penile spines—a remnant from our chimpanzee ancestors—is lacking in Neanderthal and Denisovan genomes, just as it is in modern humans, suggesting that it vanished from our ancestral hominid past at least 800,000 years ago. This is significant, as penis spines are thought to be beneficial in promiscuous species, where they may help males compete and maximize their reproduction odds. This has led to speculation that Neanderthals and Denisovans were monogamous by nature, just as humans generally promote monogamy as a virtue across cultures.
The Last Neanderthal: End of the Line
Crossbreeding with Neanderthals has likely contributed to a range of traits found in modern humans, from skin tone, hair color, and height to our sleeping patterns, and even our immune systems. Learning about them is already leading to potential treatments for modern diseases, such as drugs that target a Neanderthal gene thought to contribute to severe cases of CoViD-19.
The extinction of Neanderthals is thought to have occurred about 40,000 years ago. And there is some conjecture that STDs may have played a part. In fact, one theory promotes the view that diseases carried by the two subspecies—such as HPV and herpes—initially formed an invisible barrier, preventing either from expanding their territory and potentially coming into contact with one another. In the few areas where they did overlap, they interbred, granting early modern humans useful immunity genes, which suddenly made it possible for them to engage in territorial expansion.
Neanderthals, on the other hand, had no such luck, since, if they were saddled with a higher burden of disease to begin with, they may have remained vulnerable to these exotic new strains for a longer period, leaving them stuck, not only geographically, but in a biological bottleneck evolution-wise. Eventually, the ancestors of present-day humans invaded their territories and exterminated them.
Another theory holds that we gradually assimilated their relatively small population into that of early modern humans. After all, they had already largely adopted our Y chromosomes and mitochondria, and at least 20% of their DNA can still be found in modern humans.xii
Further studies on the genetic component of CoViD-19 susceptibility has revealed that five genes in particular exacerbate the likelihood of a CoViD-19 patient being admitted to the ICU and dying. A recent study conducted by the University of Edinburgh gathered DNA from 2,700 CoViD-19 patients in 208 ICUs across the UK. These were some of the most severe cases of CoViD-19 infection, as 22 percent of patients studied died, with 74 percent requiring ventilators, finding themselves unable to breathe on their own. The genetic information of these patients was compared to 100,000 anonymous Britons, revealing five common genes among extremely severe cases.
Knowing which genes are involved in severe cases of CoViD-19 infection can help scientists identify pre-existing drugs that could help treat CoViD-19. In addition, knowing which genes are involved in severe CoViD-19 cases could help identify which pre-existing drugs could be reassigned to fight the disease.
Revealed: The Five Genes
Creates an enzyme that can lead to inflammation. It is targeted with JAK inhibitors, which is facilitated by a drug already approved for use in humans called baricitinib, which was originally developed to treat rheumatoid arthritis.
It can be targeted by drugs that are undergoing trials, but have been used for psoriasis in the past. Evidence for this gene is not as strong as that found in other genes from the study, but researchers hold out some hope for the possibility.
This is a gene that initiates a signal that activates an enzyme which degrades RNA derived from viruses. Several other coronaviruses have a way of impeding the function of this mechanism. There is no tangible evidence yet that this is the case for SARS-CoV-2, but it might constitute a specific feature capable of doing this. It is targeted by a class of drugs called phosphodiesterase 12 inhibitors. While they are not currently being tested in clinical trials, they theoretically could enhance the antiviral effects of this mechanism.
This is a core part of signalling that initiates the host antiviral response. Signalling in this pathway is linked to the cause of sickness, which could help fight the virus directly, much like OAS1. It is important to facilitate this early in onset of the disease, as in later stages, virus levels drop, and the problem to be addressed is autoimmune dysfunction.
While DPP9 is known to contribute variously to inflammation, researchers do not yet know exactly where it fits in terms of CoViD-19 disease progression, finding they are unable to make a direct therapeutic prediction at this point. It is associated with pulmonary fibrosis and might be associated with a phenomenon known as “long CoViD.”
1. The genes were identified across the genome, with two on chromosome 19 called TYK2 and DPP9 and one found on chromosome 21 called IFNAR2.
CCR2 is a gene found on chromosome four, while OAS1 is located on chromosome 12. The prevalence of these genes partly explains why some people become extremely sick with CoViD-19, while others remain virtually unaffected. The importance of this study is that it identifies specific genes that play a role in CoViD-19 susceptibility, exposing them as targets for potential treatments. All five of the genes fall into one of two groups: modulators of inflammation or antivirals, the latter impeding the virus’s ability to replicate in the body.
In severe cases of CoViD-19, the virus levels have often already dwindled, and most of the damage is caused by a malfunction in the body’s immune system, causing it to attack the lungs and trigger severe inflammation, which sounds ominously like an autoimmune disease response, leading to a cytokine storm.
The closest thing to a cure for this severe immune reaction is dexamethasone, a steroid which has been known to save approximately 35 percent of patients relying on ventilators for respiratory assistance. One of the inflammatory genes is TYK2, which was identified by researchers as being a prime candidate for future clinical trials.
As part of the study, researchers performed Mendelian randomization, which allowed them to simulate a clinical trial. The researchers used this to compare people with differing levels of TYK2 expression, finding that people who produced more TYK2 are more at risk of CoViD-19 infection.
It has been discovered that, if production of the enzyme produced by TYK2 should happen to go awry, it can lead to excessive inflammation following CoViD-19 infection, which can often be fatal. The discovery of TYK2’s involvement in CoViD-19 is key, as there is a pre-existing drug called baricitinib that targets it. Known as a JAK inhibitor, baricitinib has already been approved for fighting rheumatoid arthritis. Researchers think JAK inhibitors could be of benefit to CoViD-19 patients by reducing the threat of lung inflammation.xiii
Washington University School of Medicine in St. Louis is a genome sequencing center undertaking a study to sequence the DNA of young, healthy adults, and children who develop severe CoViD-19. The researchers are looking for genetic defects that could put certain individuals at greater risk from CoViD-19. Researchers also intend to study people who seem immune to CoViD-19, despite repeated exposure. Such people may have genetic variations that act as an immune firewall for the virus. For example, certain rare genetic variants are known to prevent some types of viral infections, including HIV and the norovirus. Knowledge gained from understanding CoViD-19’s challenges, including its pathogenicity and resistance capability, could lead to new therapies for combatting the illness.
“The first focus of our study will be patients with severe responses to SARS-CoV-2 infection—severe enough to require intensive care—who appear otherwise healthy and are younger than 50,” said Dr. Cooper, head of the clinical immunology program at St. Louis Children’s Hospital.
“These patients don’t have uncontrolled diabetes, heart disease, chronic lung disease or any other condition that we know increases the risk of severe complications from CoViD-19,” she said. “For example, we sometimes see stories about, say, a marathon runner or a generally fit, healthy person who nevertheless got very sick from this virus, or the few healthy children who are getting very sick with CoViD-19. These are the kinds of patients we’re interested in for this study. A small proportion of hospitalized patients will fit this category, likely less than 10%.”
Cooper studies primary immunodeficiencies in children, comprising some 450 genetic disorders of the immune system, often caused by gene mutations that have an impact on different aspects of immunity.
“With this pandemic, we can use our skills in gene hunting to search for genes that might be associated with severe CoViD-19 in children and younger adults,” she said. “We can foresee a future ability to do a genetic sequencing test for individual patients hospitalized with SARS-CoV-2 and get an idea of whether they are likely to need more intensive care. In the meantime, we will be able to learn a great deal about how the immune system responds to this virus and what it needs to be able to respond effectively and in an appropriate manner.”
The study of CoViD patients’ genetics could reveal the important immune mechanisms used by the body to fight the virus. This could lead to the development of therapies that could help other patients with no genetic susceptibility to the virus, but who may have high-risk conditions, such as diabetes or heart disease.
“Our immune systems have never seen this virus before,” Cooper said. “We’re seeing severe CoViD-19 complications play out across the world right now. It is going to take a global effort to investigate the genetic factors and the immune system factors that really control this infection.”xiv
How Some Show No Symptoms While Others Become Deathly Ill
A study in Nature of more than 2,200 intensive care patients has identified specific genes that may hold the answer to how some show no symptoms while others become deathly ill. The presence of these genes appears to make some people more susceptible to severe CoViD-19 symptoms. The discovery sheds light on inherent weaknesses in the immune system, which could lead to new treatments.
These will continue to be needed even though vaccines are being developed, says Dr. Kenneth Baillie, a consultant in medicine at the Royal Infirmary in Edinburgh, who led the Genomic project. “Vaccines should drastically decrease the numbers of CoViD cases, but it’s likely doctors will still be treating the disease in intensive care for a number of years around the world, so there is an urgent need to find new treatments.”
Scientists examined the DNA of patients in more than 200 ICUs in UK hospitals. They scanned each patient’s genes, which contain instructions for every biological process, including how to fight deadly antigen such as viruses. Their genomes were then compared with the DNA of healthy people to see what genetic differences could be identified. The scientists managed to pinpoint a number of genetic dichotomies, the most prominent of which was a gene called TYK2. “It is part of the system that makes your immune cells more angry, and more inflammatory,” explained Dr. Baillie.
It was soon discovered that, due to this faulty gene, it was possible for the immune response to spawn an autoimmune dysfunction, which could put some patients at risk of damaging lung inflammation. A class of anti-inflammatory drugs already used for conditions such as rheumatoid arthritis targets this biological mechanism, including a drug called baricitinib. “It makes it a very plausible candidate for a new treatment,” Dr. Baillie said. “But of course, we need to do large-scale clinical trials in order to find out if that’s true or not.”
Too Little Interferon
Other genetic differences were pinpointed, including one found in a gene called DPP9, known to play a role in inflammation, and also in a gene called OAS, which helps stop the virus from making copies of itself. Variations were also discovered in a gene called IFNAR2 in patients in the ICUs.
IFNAR2 is linked to a potent anti-viral molecule called interferon, which helps the immune system mobilize as soon as an infection is detected. It is believed that weak interferon production could give the virus a head start, allowing it to quickly replicate, leading to more severe disease.
Two other studies published in the journal Science have implicated interferon in CoViD-19 cases, as a result of both genetic mutations and an autoimmune disorder that affects its production. Professor Jean-Laurent Casanova, who carried out the research, from The Rockefeller University in New York, said: “[Interferon] accounted for nearly 15% of the critical CoViD-19 cases internationally enrolled in our cohort.”
Interferon can be given as a treatment, but a clinical trial conducted by WHO concluded that it was of little benefit to chronically sick patients. However, Professor Casanova indicated that the timing was important: “I hope that if given in the first two, three, four days of infection, the interferon would work, because it essentially would provide the molecule that the [patient] does not produce by himself or by herself.”
Dr. Vanessa Sancho-Shimizu, a geneticist from Imperial College London, said these genetic discoveries were significant in terms of understanding the biology of the disease. “It really is an example of precision medicine, where we can actually identify the moment at which things have gone awry in that individual,” she said. “The findings from these genetic studies will help us identify particular molecular pathways that could be targets for therapeutic intervention.”
The researchers identified a cluster of genes on chromosome 3 strongly linked to severe symptoms. However, the precise biological explanation for this is not yet known. More patients are being encouraged to participate in this study. “We need everyone,” said Dr. Baillie, “but we’re particularly keen to recruit people from minority ethnic groups who are over-represented in the critically ill population. There’s still a very urgent need to find new treatments for this disease and we have to make the right choices about which treatments to try next, because we don’t have time to make mistakes.”xv
What is not being discussed by these researchers, because of political correctness interfering with objective science is the reason there is an overrepresentation of ethnic minorities experiencing immune response complications resulting from CoViD-19 infection. The answer can be found in their genomes, but is not being discussed. The problem is related to the gene TYK2, which makes immune cells angrier, resulting in inflammation. This occurs in patients that have a higher ratio of Neanderthal and Denisovan genetics. This suggests that the virus is chewing at the low end of the evolutionary tree. Since Europeans have developed mechanisms to prevent this, probably as a result of the European population being survivors of the Bubonic Plague that wiped out two-thirds of the inhabitants of the continent, allowing them to develop an immune component resistant to plague relatives like coronaviruses. The fact is that due to the spike proteins associated with SARS-CoV-2, the virus tends to imbed itself in healthy cell tissue, arterial walls, heart, lung, and other vital organs, so that when antibodies mobilize an attack against the invading antigen, they damage the vital organs, artery walls, and healthy tissue in the process. This is a direct result of the TYK2 gene complication, which is more prevalent in patients with a higher Neanderthal and Denisovan gene expression. As politically incorrect as it may be, this gene expression has been found to be more prevalent in so-called ethnic minority groups found in Western developed countries, i.e. South Asians with a 60% Neanderthal gene component, Far East Asians with a strong Denisovan genetic component, some pockets of African populations who have inherited Neanderthal genetics from waves of migrations originating in the Altai Mountains. Where the problem is particularly pronounced is Brazil, where the native population, with a high Denisovan gene expression, have bred with those of African descent, and influxes of other populations with a high Neanderthal gene expression. This has quadrupled the TYK2 gene expression problem, resulting in autoimmune disease dysfunction.
Obesity Doubles the Risk of CoViD-19 Infection and Mortality
If the problems already identified weren’t enough, U.S. researchers have found that obesity makes people more prone to other diseases such as diabetes and high blood pressure, which in turn weakens their immune system. Due to their compromised immune system, such people become more susceptible to severe CoViD-19.
Researchers also believe that vaccines would prove less effective in protecting obese patients from CoViD-19 also because of the problem of weak immunity, as flu vaccines have been found to be less effective in those with a body mass index (BMI) of over 30.
The team from the University of North Carolina reviewed a total of 75 studies from around the world, including nearly 400,000 patients, and found that CoViD-19 patients suffering from obesity were twice as likely to be hospitalized and 74% more likely to be admitted to ICU. They were also found to be more at risk of dying from CoViD-19 infection.
Professor Barry Popkin, who led the study, said the increased risks of being obese and having CoViD-19 were “much higher than expected.” Obesity has been linked to a number of diseases that make people more susceptible to a severe reaction to CoViD-19 infection. It was found that obesity heightens the danger of bodily inflammation, reduced immune response, and increased stress for vital organs, including those involved with respiration.
“Vaccine researchers should look at how it affects obese individuals,” Professor Popkin says of a CoViD-19 vaccine. He is concerned that vaccines could prove deadly in populations with a high percentage of obese people. With 20% of the population overweight or obese in most countries–nearly 60% in the UK and U.S.–understanding how the obese might react to treatments and vaccines is “critical”.xvi
To substantiate the argument, the majority of CoViD-19 deaths internationally have occurred in countries with a ratio of obesity, with coronavirus fatality rates 10 times higher in nations where at least 50% of adults are overweight, according to a global study.
The report established a dramatic correlation between CoViD-19 death and obesity rates in countries around the world, finding that 90% or 2.2 million of the 2.5 million CoViD-19 deaths were in countries with high obesity rates. The study was based on CoViD-19 death figures compiled by Johns Hopkins University in the U.S. and the WHO’s Global Health Observatory data on obesity. “Look at countries like Japan and South Korea, where they have very low levels of CoViD-19 deaths as well as very low levels of adult obesity,” said Tim Lobstein, an expert advisor to the World Obesity Federation, who co-led the report. “They have prioritised public health across a range of measures, including population weight, and it has paid off in the pandemic.”
By contrast, the report found that in the U.S. and UK, there was a clear correlation between high CoViD-19 death rates and obesity levels. The UK has the world’s third-highest CoViD-19 death rate and the fourth-highest obesity rate—184 CoViD-19 deaths per 100,000 in a population with 63.7% of adults overweight, according to WHO data—followed by the U.S., with 152.49 CoViD-19 deaths per 100,000 in a population top heavy with 67.9% obese adults.
John Wilding, a professor of medicine at Britain’s University of Liverpool and president of the World Obesity Federation, sees obesity as a key factor in CoViD-19 health risk and believes it should be given serious consideration in the development and deployment of vaccines.
“It’s really important that we recognise that obesity…increases the risk,” he said in a statement about the report’s findings. “Therefore, like other diseases such as diabetes and cardiovascular disease, people with obesity should be considered for early priority in vaccination programmes across the world.”xvii
This is actually a dangerously misguided statement for John Wilding to make, since the CoViD-19 vaccine could prove deadly if given to the obese, particularly the mRNA vaccines developed by Pfizer and Moderna, precisely because these vaccines program messenger RNA to produce the same spike proteins found in the virus itself, ostensibly so as to mobilize the immune system to attack the SARS-CoV-2 virus if it ever shows up. However, it has been found that the vaccine is likely to induce the same autoimmune disease dysfunction that the virus itself causes due to the fact that spike proteins tend to imbed themselves in blood vessel walls, as well as heart and lung tissue, prompting antibodies to attack these very sites.
It has been noted that as far as the first year of the pandemic is concerned, CoViD-19 hit some parts of the world harder than others. As of Oct 22, 2020, it was found that the top 23 countries ranked by death rate per 100,000 population were either in the Americas or Europe. The mortality rate can be strikingly different depending on the country. For example, Taiwan and Vietnam have had only 0.03 and 0.04 deaths per 100,000 respectively, whereas the 23 top countries all have a death rate greater than 38 per 100,000—a factor of 1000 or three orders of magnitude greater.
One factor that has been overlooked in CoViD-19 mortality statistics is the impact of chronic glyphosate exposure. Glyphosate is the active ingredient in the widely used herbicide Roundup, formerly used by Monsanto, but still in use by other agro-giant entities. Commonly used to control weeds in large industrialized farms, it is also used as a desiccant just before harvest. It has become clear that a number of comorbidities such as diabetes, hypertension, and obesity exacerbate the illness in CoViD-19 patients. In the U.S., these chronic diseases are rising in proportion with the increased use of glyphosate on core crops. Glyphosate has been identified as a key factor in making the CoViD-19 pandemic more chronic.
Most concerning is the possibility that glyphosate is released into the atmosphere as a by-product of the biofuel industry. The U.S., Brazil, Argentina, and most European countries have all played a leading role in developing technology aimed at turning food industry waste into useful fuel. Such fuel sources include plant stocks left behind after the harvest, manure, and by-products of the meat-processing industry, waste oil from restaurants, and wood scraps from the paper-manufacturing industry. All of these can contain glyphosate contaminants. Cities with a high usage of biodiesel, biofuel for heating oil, aviation biofuel, bioethanol, and/or biogas are likely to be badly impacted by CoViD-19, because glyphosate exposure through breathing disrupts immune function in the lungs, interfering with the patient’s ability to purge the virus.
Chemtrails are a related factor, as they contain barium, strontium, aluminum and other elements known to be immune suppressants. While there are claims that chemtrails are part of a geoengineering effort to reduce global warming by reflecting some solar radiation back into outer space, the secrecy and lack of disclosure about the true purpose of chemtrails suggest it is more probably part of a multipronged attack on the population as part of an effort to cull the herd. Unfortunately, we are being bombarded with chemical additives in our food and water, and air particulate elements in air pollution, that dramatically reduce our immune response when diseases like CoViD-19 show up.
There are many factors exacerbating the seriousness of the CoViD-19 pandemic. One often overlooked issue is the role of element deuterium, which is central to the disease process. Proper deuterium fractionation is crucial for metabolism to work properly in the cellular organelle known as the mitochondria. Water accumulating in the lungs—a common feature of CoViD-19—is an active attempt to restore mitochondrial health to the immune cells, which may be an expression of edema anywhere in the body it is demonstrated to occur.
Professor László Boros has done extensive research on the damaging effects that deuterium has on mitochondria. Deuterium is a heavy hydrogen isotope. Hydrogen is the smallest atom, with only one proton and one electron. Deuterium is atomically nearly the same, except that it has an extra neutron, making it almost twice as heavy as hydrogen, while granting it distinct physical and chemical properties. Deuterium is quite pervasive in nature, found at 155 parts per million in seawater for instance. Mitochondria are small organelles contained in large numbers in most eukaryotic cells, and they are responsible for producing adenosine triphosphate (ATP), the major energy source for cells. When cells create ATP, they also combine protons with oxygen to produce water.
Systemic mitochondrial deterioration is one of the major indicators of the aging process. Mitochondrial dysfunction, caused by glyphosates raising deuterium levels, has been linked to many neurological, metabolic, and oncological diseases, as aged mitochondria spew out more tissue-damaging waste products and produce ATP less efficiently. Mitochondria depend upon a “proton motive force” to produce ATP, which involves pumping huge quantities of protons across a membrane through the ATPase pump. As deuterons are larger and heavier than hydrogen atoms, they disrupt the smooth flow of protons and decrease the efficiency of the pump, disrupting the fuel line like putting sugar in a gas tank.
Glyphosate and Deuterium
A unique aspect of glyphosate’s cumulative toxic buildup is its ability to get inserted into proteins by mistake in place of the coding amino acid glycine. Glycine is the smallest amino acid. Glyphosate is a complete glycine molecule, except that it has an extra methylphosphonate unit attached to its nitrogen atom. The enzyme that glyphosate disrupts in organisms has a glycine residue. Species that have a mutated form of the enzyme—with alanine replacing this glycine residue—are completely immune to the effects of glyphosate. Without glycine, there is no chance to substitute and disrupt the protein. Sulfate supplies can also be depleted by glyphosate, which disrupts the organism’s ability to maintain adequate amounts of gelled water. Glyphosate is known to disrupt sulfate synthesis, transport, and transfer from one molecule to another.
One CoViD-19 study used computational techniques to analyze “gene expression data from cells in bronchoalveolar lavage fluid (BALF) from CoViD-19 patients that were used to sequence the virus.” Their technique allowed them to determine which proteins were overexpressed in the alveoli in the lungs of infected patients. They found that a protein called bradykinin was produced in large amounts in the infected lungs. Bradykinin is a powerful signaling molecule, producing a drop in blood pressure and inducing leakages in the blood vessels that allow both immune cells and fluid to escape from the blood and enter the interstitial spaces. In addition, they found overproduction of hyaluronic acid in the lung alveoli. Through osmosis, hyaluronic acid attracts and impedes the fluid escaping from the blood, inducing pulmonary edema, a characteristic feature of ARDS (acute respiratory distress syndrome). This explains why many CoViD-19 patients experience a sensation very similar to drowning. By trapping gelled water, the hyaluronic acid creates a negatively charged gel that releases protons into the interstitial spaces, in order to fuel the mitochondria of cells.
Viral Lipid Envelope and Lipoxygenase
Remarkably, it has been discovered that the SARS CoV-2 virus protein coat contains three pockets within its contour shape that perfectly fit a very common fatty acid called linoleic acid. It is surmised that the virus picks up multiple molecules of linoleic acid as it exits the human host cell, surrounding itself with a lipid envelope. Since the immune cells respond to the virus by inducing an inflammatory response, and an inflammatory response induces lipoxygenase, it is probable that the linoleic acid trapped in the membranes of the viruses will be metabolized by lipoxygenase to produce leukotrienes, while also further supplying DDW to the surrounding fluids. This sets up a perfect storm for macrophages (“big eaters”—immune cells that specialize in clearing viruses) to congregate at the site of the immune response to the virus. This can have the disastrous effect of causing auto-immune disease dysfunction, since the over-accumulation of such macrophages can spawn an attack in certain undesirable sites such as the heart muscle of lung tissue.
It has only recently become known to researchers that cells have a remarkable ability to share mitochondria, and that this practice can lead to a healing process for sick immune cells. An acute reaction to SARS CoV-2 results in an intense inflammatory response that sets in motion a dramatic sequence of events, possibly with the ultimate goal of energizing the macrophages so that they can effectively clear the virus. Glyphosate appears to be a major culprit in obstructing this process. If the immune cells were healthy, they would easily clear the virus without overt symptoms of disease.
Besides mesenchymal stem cells, platelets are also a fantastic source of fresh mitochondria for the macrophages. Platelets are tiny cell fragments with no nucleus, each containing a handful of mitochondria. Under stressful conditions, so-called “activated” platelets release their mitochondria, either as isolated mitochondria or packaged up inside lipid particles called exosomes. The macrophages take up these mitochondria, most likely after they have been re-enforced with deuterium depleted water. In fact, one of the primary functions of platelets may be to serve as a reserve supply of healthy mitochondria for the immune cells.
It would seem that the virus has facilitated a remarkable repair mechanism, which empowers the macrophages to clear the virus, because they have now been endowed with an adequate supply of healthy mitochondria. This creates a very different viewpoint on the role viruses play in health and disease. The viruses appear to be collaborating with host cells in a symbiotic relationship that results in healing, unless too many toxic impediments should undermine this process. We should remember that mitochondria are thought to be viral stowaways that ended up taking up permanent residence within the cells of eukaryotic species. This explains why mitochondria produce their own RNA and DNA as organelles within the cell.
Drastic Final Measures
In some patients, the mitochondria in their macrophages may become impaired due to chronic glyphosate exposure. When this happens, a systemic response ensues, involving the entire circulatory system. What occurs is that production of an enzyme called heme oxygenase is massively increased in response to low oxygen levels, breaking down the heme found to be present in large amounts in the red blood cells, converting it to biliverdin. Biliverdin, in turn, gets converted to bilirubin, an effective antioxidant that can guard against oxidative damage caused by free radicals. But, for every molecule of biliverdin produced, there will be three molecules of deuterium depleted water. It has been shown that heme oxygenase is a welcome response to inflammation, which eventually tames the inflammation and resolves the disease. However, glyphosate can interfere with this process as well, resulting in a harmful positive feedback loop and a relentless chain reaction of inflammation. Ultimately, massive blood clots form throughout the capillaries and the patient dies from blood clotting or from multiple organ failure.
Research papers on the course of the CoViD-19 disease reveal a remarkable mechanism by which a serious mitochondrial disorder in the immune cells can actually be repaired by SARS CoV-2. At first, the patient experiences the uncomfortable sensation of drowning due to the accumulation of deuterium depleted water in the lungs. However, this water enables the macrophages to repair their mitochondria, empowering them to clear the virus, metabolizing the viral components into useful raw materials. Remarkably, it actually has the effect of strengthening the host’s immune system.
But this may not be enough for patients who have been more severely compromised by glyphosate and other environmental toxins. These patients tend to progress into a more severe stage where platelet involvement can result in serious blood clots in the vascular system, with potentially life-threatening consequences. It may be deduced, therefore, one may be able to protect oneself from CoViD-19 by consuming a 100% certified organic whole foods diet.xviii
Quite remarkably, scientists have discovered that some recovering CoViD-19 patients did not appear to have any antibodies against it. It was then discovered that, many of those who developed antibodies against the virus, seem to lose them again within a few months. In short, though antibodies have proved invaluable for tracking the spread of the pandemic, they might not play as active a role in immunity as scientists once thought. Long-term protection may depend on other variables than simple antibody immunity.
While virologists remain preoccupied with the role played by antibodies, researchers realize that another form of immunity may play a role, one that has been lurking undetected in the body for years. An enigmatic type of white blood cell is achieving greater notice. And though it has not previously featured heavily in the public consciousness, it may well prove to be crucial in our fight against CoViD-19. T-cells may steal the limelight soon given the change in focus that has made it assume center stage.
Blood Samples Show T-cells Detect Proteins on CoViD-19 Virus Surface
A T-cell is a kind of immune cell, whose main purpose is to identify and hunt down invading pathogens or infected cells and kill them. It does this using proteins on its surface, which can bind to proteins on the surface of viruses. Each T-cell is highly specific. There are trillions of possible versions of these surface proteins, each capable of recognizing a different target. Because T-cells can linger in the blood for years after an infection, they also contribute to the immune system’s “long-term memory,” helping it mount a faster and more effective response whenever a slight variant of an old nemesis turns up.
Several studies have shown that people infected with CoViD-19 tend to have T-cells capable of targeting the virus irrespective of whether they have experienced symptoms. However, scientists have also discovered that some people can test negative for antibodies against CoViD-19 and positive for T-cells with the capability of identifying the virus. This has spurred the theory that some level of immunity against the disease are more common than previously thought.
Quite surprisingly, when researchers tested blood samples taken years before the pandemic started, they found T-cells specifically tailored to detect proteins on the surface of CoViD-19. This suggests that some people had already developed an immune mechanism resistant to the virus before it had even appeared. In fact, this phenomenon of pre-existing immunity appears to be surprisingly prevalent: 40-60% of unexposed individuals had these cells. It looks increasingly as if T-cells might afford a secret form of immunity to CoViD-19.
The central role of T-cells could also help to explain some of the anomalies that have so far defied explanation—from the dramatic escalation in risk older people face when confronted by the virus, to the shocking discovery that it can destroy the spleen. Deciphering the importance of T-cells is not just a matter of academic curiosity. If scientists know which aspects of the immune system are most important, they can direct their efforts to devising more effective medicinal remedies.
How Immunity Works
Most people probably have not considered the role played by T-cells or T-lymphocytes as they are also known, but to see just how crucial they are to our immune response, we only have to look to late-stage AIDS. While the persistent fevers, sores, fatigue, weight loss, rare cancers have begun to manifest, normally harmless microbes, such as the fungus Candida albicans—usually found on the skin—start to take over the body.
Over the course of months or years, HIV mobilizes a reconnaissance and subterfuge campaign against T-cells—factory cells that manufacture the body’s defenses—invading them and sabotaging them from within so that they commit suicide. “It wipes out a large fraction of them,” says Adrian Hayday, an immunology professor at King’s College London and group leader at the Francis Crick Institute. “And so that really emphasises how incredibly important these cells are—and that antibodies alone are not going to get you through.”
During a normal immune response, the first line of defence is the innate immune system, involving the leukocytes and chemical signals that raise the alarm. This engages the production of antibodies, which are triggered a few weeks later.
“And in parallel with that, starting out about four or five days after infection, you begin to see T cells getting activated, and indications they are specifically recognising cells infected with the virus,” says Hayday. These unlucky cells are then dispatched quickly and brutally—either directly by the T-cells themselves, or by other parts of the immune system they coopt to accomplish the task for them. All this occurs before the virus has a chance to turn them into factories that produce more copies of itself.
What Is Known about T-Cells and CoViD-19?
“Looking at CoViD-19 patients—but also I’m happy to say, looking at individuals who have been infected but did not need hospitalisation—it’s absolutely clear that there are T cell responses,” says Hayday. “And almost certainly this is very good news for those who are interested in vaccines, because clearly we’re capable of making antibodies and making T cells that see the virus.”
In fact, one vaccine developed by Oxford University in collaboration with AstraZeneca has already been shown to trigger the production of these cells in addition to antibodies. It is still too early to know how effectively this will boost the immune response, but its developers regard it as “extremely promising.”
There is a catch, however. In many patients who are hospitalized with more serious cases of CoViD-19, the T-cell response has been shown to be quite insipid. “Vast numbers of T-cells are being affected,” says Hayday. “And what is happening to them is a bit like a wedding party or a stag night gone wrong—I mean massive amounts of activity and proliferation, but the cells are also just disappearing from the blood.”
One theory is that these T-cells are just redirected to where they are needed most, such as the lungs, extirpated from certain areas of the body, like an extirpated species vacating its usual habitat. But his team suspects that a lot of them are dying instead, like a species experiencing an extinction die-off in the wild. “Autopsies of CoViD-19 patients are beginning to reveal what we call necrosis, which is a sort of rotting,” he says. Apparently, this is particularly evident in areas of the spleen and lymph glands which is the T-cells natural habitat within the body.
Quite disturbingly, spleen necrosis is a hallmark of T-cell disease, in which the immune cells themselves are attacked. “If you look in post-mortems of Aids patients, you see these same problems,” says Hayday. “But HIV is a virus that directly infects T-cells, it knocks on the door and it gets in.” In contrast, there is no evidence to date that the CoViD-19 virus is capable of the same feat.
“There are potentially many explanations for this, but to my knowledge, nobody has one yet,” says Hayday. “We have no idea what is happening. There’s every evidence that the T cells can protect you, probably for many years. But when people get ill, the rug seems to be being pulled from under them in their attempts to set up that protective defence mechanism.”
Dwindling T-cells might also provide an explanation for why the elderly are much more severely affected by CoViD-19 than younger populations. Hayday points to an experiment conducted in 2011, which involved exposing mice to a version of the SARS-CoV virus responsible for causing SARS. Previous research had shown that the virus, also a coronavirus and a close relative of CoViD-19, triggered the production of T-cells, which were responsible for clearing the infection.
The follow-up study produced similar results, but the twist was that this time the mice were allowed to grow old. As they did, their T-cell responses became significantly weaker. However, in the same experiment, scientists also exposed mice to a flu virus. In contrast with those infected with CoViD-19, the mice managed to maintain their T-cell defenses against influenza pretty much till the end of their life cycle.
“It’s an attractive observation, in the sense that it could explain why older individuals are more susceptible to CoViD-19,” says Hayday. “When you reach your 30s, you begin to really shrink your thymus [a gland located behind your sternum and between your lungs, which plays an important role in the development of immune cells] and your daily production of T-cells is massively diminished.”
What is the Effect on Long-Term Immunity?
“With the original [SARS] virus [which emerged in 2002], people went back to patients and definitely found evidence for T-cells some years after these individuals were infected,” says Hayday. “This is again consistent with the idea that these individuals carried protective T cells, long after they had recovered.”
The fact that coronaviruses can lead to lasting T-cell development is what recently inspired scientists to check old blood samples taken from people between 2015 and 2018 to see if they contained any T-cells capable of recognizing CoViD-19. When this was confirmed, it led to suggestions that their immune systems learnt to recognize it due to past encounters with cold viruses with similar surface proteins. This raises the tantalizing possibility that the reason some people experience more severe infections is that they are not endowed with T-cells capable of recognizing the virus. “I think it’s fair to say that the jury is still out,” Hayday maintains.
Unfortunately, no one has ever verified whether people manufacture T-cells against any of the coronaviruses that give rise to the common cold. “To get funding to study this would have required a pretty Herculean effort,” says Hayday. Research into the common cold went out of fashion in the 1980s, after the field stagnated and scientists began to migrate to other projects that seemed more important, like studying HIV. Making progress since then has proven difficult, because the illness can be caused by hundreds of different viral strains, many of them able to mutate quite quickly.
Will This Lead to a Vaccine?
If old exposures to cold viruses really do lead to milder cases of CoViD-19, this bodes well for the development of a vaccine, since it proves that lingering T-cells can provide significant protection, even years afterward. Hayday explains that the way vaccines are designed generally depends on the kind of immune response scientists are aiming for. Some might trigger the production of antibodies—free-floating proteins capable of binding to invading pathogens and either neutralizing them or tagging them so another part of the immune system can target them, similar to terrorists being tagged with a homing device so they can be targeted later. Others might aim to get T-cells involved, or perhaps provoke a response from other parts of the immune system.
“There really is an enormous spectrum of vaccine design,” says Hayday. He’s particularly encouraged by the fact that the virus is evidently highly visible to the immune system, even in those who are severely affected. “So if we can stop whatever it’s doing to the T-cells of the patients we’ve had the privilege to work with, then we will be a lot further along in controlling the disease.”
The role T-cells play in immunity is likely to get increasing attention in the future. What is clear from this most recent world pandemic is that it has redirected focus to the immune system itself, with the intention of finding ways to enhance its capability and defensive power.xix
Coronavirus Makes Changes That Cause Cells Not to Recognize It
A new study has revealed that CoViD-19 has the unique characteristic of being able to change the appearance of its messenger RNA cap to trick the host cell into not recognizing it as a foreign body. As with an alarm code that makes it possible to breach the security features of a building without setting off the alarm, SARS-CoV-2 has the same advantage when entering cells. It has the security code that grants it access.
Researchers at The University of Texas Health Science Center at San Antonio (UT Health San Antonio) explain how CoViD-19 achieves this. The scientists resolved the structure of an enzyme called nsp16, which the virus produces and then uses to modify its messenger RNA cap, said Yogesh Gupta, Ph.D., the study’s lead author. “It’s a camouflage,” Dr. Gupta said. “Because of the modifications, which fool the cell, the resulting viral messenger RNA is now considered as part of the cell’s own code and not foreign.”
Deciphering the 3D structure of nsp16 opens the door for the design of antiviral drugs for CoViD-19 and other emerging coronavirus infections, Dr. Gupta said. The new small molecule (NSM) drugs would inhibit nsp16 from making the modifications. The immune system would then be able to pick the invading virus up on its radar, recognize it as foreign, and hunt it down.
“Yogesh’s work discovered the 3D structure of a key enzyme of the CoViD-19 virus required for its replication and found a pocket in it that can be targeted to inhibit that enzyme. This is a fundamental advance in our understanding of the virus,” said study coauthor Robert Hromas, MD, professor and dean of the Long School of Medicine.
In lay terms, messenger RNA can be described as a courier of genetic code to worksites that produce proteins. If this process can be inhibited and thwarted in the virus, it could undermine the most basic component in its weapon arsenal, the main cloaking device it employs to invade and attack the human host.xx
CoViD-19 is continuing to spread across the world with 75 million confirmed cases in 190 countries and an estimated two million deaths by the end of 2021. However, these stats need to be questioned, since a lot of hospitals have been encouraging relatives of the deceased to sign death certificates attributing death to CoViD-19, as the hospitals and sometimes the relatives of the deceased receive financial incentives to do so. When you think about families who have been out of work for months due to the lockdown, a financial incentive of $2,000 or $3,000 could be a strong temptation when incurring funeral costs and other expenses. This is not a rare occurrence, but a quite common one around the world. The author of this article has directly come across two cases of patients dying from other causes having their surviving family encouraged to sign death certificates attributing the cause of death to CoViD-19. One case involved family of the author in the Philippines. Following the death of an aunt from lung cancer, the hospital authorities encouraged the family to verify CoViD-19 as the cause of death as they would receive a 37,000 pesos financial incentive for doing so. Being cash-strapped from the lockdown and faced with having to cover funeral expenses, the family felt they had no choice. It is not by coincidence that such financial incentives have been put in place or that people have been placed in such financial constraints that they are tempted to accept what amounts to a bribe. Folks, this is part of the conspiracy. The fact that people have now stopped using the phrase conspiracy theory so liberally points to the fact that we are all in the midst of the greatest conspiracy ever hatched on this planet, one that is directly affecting all of us.
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Note: The recent jump and fall in the 56-day trend for global cases was caused by Turkey
Source: Johns Hopkins University, national public health agencies and UN population data
Figures last updated: December 21, 2020, 08:19 GMT
We have been led to believe that coronavirus cases have surged over the past few months in several regions of the world and a spike in new infections has been seen in many countries in early 2021. It is hard to know what to believe, when the PCR test cycles have been deliberately increased to create false positives. How many people have been intubated that were only suffering from the seasonal flu and succumbed as the result of inappropriate treatment? It is worth asking the question because the level of fraud committed during this worldwide criminal operation is unprecedented in the history of the world. It is shocking that lack of integrity and virtuosity could have brought us to this. Who could have ever believed that politicians and medical professionals could have sold us out so easily over petty financial incentives that in many cases don’t even benefit them directly and cause them to commit treason and even mass murder against their own citizens? It is shocking to see how the Nuremburg Code’s strictures against medical experimentation on civilian populations without their informed consent have been so easily flouted and how easily we have forgotten the lessons of history.
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The WHO has warned that the CoViD-19 vaccines granted approval for public use are no magic bullet for the coronavirus and present no guarantee that the pandemic will end any time soon. “Vaccines do not equal zero CoViD,” said WHO emergencies director Michael Ryan. “Vaccination will add a major, major, powerful tool to the tool kit that we have. But by themselves, they will not do the job.” Such an admission begs the question of why, when there is no evidence of any benefit to be derived from CoViD vaccination that such a dangerous form of treatment would be recommended in the first place. And given that the military-pharmaceutical complex is responsible for developing the weaponized coronavirus through gain-of-function laboratory experimentation, and that the same entity is behind the vaccines, it should be clear to anyone with a modicum of sense that we have been boxed in by a problem-reaction-solution dialectic, in which the so-called solution is likely to kill us as effectively as the problem. The only answer to this global military assault on the world’s citizenry is total non-compliance with this criminal totalitarian world and local government tyranny.
Several countries have approved CoViD-19 vaccines for use on the civilian population. The fact that vaccines have been promoted to the exclusion of all else as an antidote to CoViD-19, while alternatives are being suppressed is shocking and quite infuriating to say the least. One would have thought that citizens living in so-called democracies in Western developed countries would be granted some level of choice when it comes to deciding on personal health options. However, such choices are not being granted, and our freedoms have been stripped away to the point where we have been cajoled into a “new normal” that is far from normal, ethical, or acceptable. We have been told that it is for our own good, and that the greater good—the health and well-being of society as a whole—is the summum bonum. Meanwhile, we have all collectively lost our rights, freedom, and sovereignty, and are unlikely to ever get them back once we have naively relinquished them.
U.S. Has Most Purported Cases and Deaths
The U.S. had purportedly recorded nearly 20 million cases and more than 300,000 deaths from CoViD-19 by the end of 2020, the highest figures in the world supposedly. But are these stats reliable? With hospitals receiving financial perks for CoViD-19 patients, many are choosing to list their patients as CoViD-19 casualties, when they are nothing of the kind. Yet, we are told that daily cases have been at record levels since early November 2020, and 100,000 people are purported to have been hospitalized with CoViD-19, more than in either of the two previous waves, if the stats can even be relied upon, which is highly questionable, given the financial incentive hospitals receive for listing patients as victims of CoViD-19. In addition, there are inaccuracies in the count caused by flaws in the PCR Test Kits, which Dr. Yeaden, a scientist long associated with Pfizer, alleges is inflating CoViD-19 positive results by ten times.
There is another reason to be skeptical about the U.S. CoViD-19 statistics, which is the political factor. The World Economic Forum has made it abundantly clear through its own literature that it is opposed to the neo-liberal economic model exemplified by the UK and U.S. It therefore has a vested interest in setting both countries up for “failed nation” status due to alleged poor CoViD-19 response measures, while sabotaging the two countries’ economies through lockdown and shelter-in-place measures, while heaping praise on communist China for launching such an effective response. The leftist bias in the Western media has become so obvious that it should be clear to anyone with any powers of perception that this plandemic is a world communist coup orchestrated by the UN world government and its affiliate agencies. Even the stats are biased, while most of the so-called ‘science’ has been reduced to pseudo-science to compliment the mainstream CoViD-19 narrative promoted by mainstream media and academia.
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The outbreak has had a devastating impact on the world economy, but the U.S. economy has been hit particularly hard. Nearly eight million Americans, many of them children and minorities, have fallen into poverty since May of 2020. However, it is clear from the book COVID-19: The Great Reset by World Economic Forum founder Klaus Schwab and colleague, Theiss Milleret, that the U.S. and UK are singled out as economies that embrace neo-liberalism, which the authors see as a fault. Their observation is that the countries that mobilized the most effective response to the CoViD-19 pandemic were countries that were more command and control in economic orientation and had relatively homogenous populations that could be rallied in solidarity and common cause rather easily to respond to the ‘pandemic’ emergency. It is clear what the two co-authors favor and the kind of future society their colleagues at WEF support.
Meanwhile, it has been reported that daily cases had fallen in many European countries during November 2020 after some steep rises in October. But in December, cases had allegedly begun to surge again in several countries, including France, Germany, and the UK, so it has been reported. However, what has not been taken into account is that more testing is being conducted than before, which is naturally going to increase the stats. Even more worrying is the fact that many of the PCR tests are known for their inaccuracy and are generating many false positives. The bang on effect of this is that lockdowns are becoming more draconian in nature, and civil liberties are being stripped away by governments and health authorities that are unlikely to ever give them back. Lockdowns and other restrictions have been reintroduced in some of the worst-affected regions ostensibly to help bring down the numbers. And many countries have placed temporary bans on arrivals from the UK, because of concerns about the spread of what has been dubbed “a new variant” of the coronavirus, which may have led to a rise in cases in some parts of the country. The overall effect of all this is that our countries are being economically sabotaged, quite by design, in a strategy game consisting of “disaster economics,” so that the globalists can usher in the Great Reset, which will usher in a worldwide digital currency to replace the wilfully and deliberately bankrupted national currencies it has been designed to replace.
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What Other Places Have Seen an Infection Spike?
Asia was the center of the initial outbreak, but the number of cases there was relatively low until it saw a surge in infections over the summer of 2020, which had recorded 10 million confirmed cases at the time, the second-highest official total in the world after the U.S. The daily number then tailed off come September 2020, but has since shot up dramatically in the early months of 2021. This is probably attributable to the Neanderthal genetic fostering the gene defect TYK2, which results in immunity complications.
In Latin America, Brazil has more than 7 million confirmed cases and the world’s second highest death toll. In all likelihood, Brazil is particularly hard hit due to the combination of Denisovan genetics among the native population and the Neanderthal haplotype in those of African ancestry, magnifying the TYK2 gene defect multifold in the mixed Brazilian population. The country was purportedly experiencing a second wave of infections at the end of 2020. Argentina, Colombia, and Mexico have also recorded more than 1 million cases and all three countries were still producing high numbers of daily confirmed cases in early 2021.
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Africa has recorded about 2.5 million cases, but the true extent of the pandemic on that continent is unknown as testing rates are low. South Africa, with more than 900,000 cases and 24,000 deaths, was the worst affected country on the continent by the end of 2020. Genetics would be an obvious factor, since South Africa is particularly multicultural with a substantial population of so-called ‘colored’ people, many of whom are of Indian origin. Morocco, Egypt, Ethiopia, and Tunisia are the only other African countries to officially record more than 100,000 cases.
What about the Economic Toll?
Governments around the world have chosen to limit public movement and close businesses and venues in a bid to slow the virus’s spread. This has had a devastating impact on the global economy. Damage to the world’s major economies is four times worse than the 2009 global financial crisis, according to the Organization for Economic Cooperation and Development (OECD). Meanwhile, the UN has said that up to 265 million people could face starvation by the end of the year because of the impact of the CoViD-19 lockdown. The UN also admits that the ‘pandemic’ could also wipe out 25 years of improvements in gender equality. The UN and its affiliate totalitarian world government bodies can congratulate themselves for these achievements, since they are wholly and entirely to blame for this human tragedy.
Given the UN projection on the harm caused by pandemic lockdowns, one wonders at the wisdom of a worldwide response protocol that is actually increasing rather than decreasing the deathrate. Given that at least 265 million people are projected to be suffering from starvation, it is clear that the lockdown will be responsible for more suffering and death than the virus itself. From that perspective, it seems clear that the UK government might have been right all along when it adopted a policy of allowing herd immunity through a laisser-faire approach to virus spread.xxi
Gauging the true extent of the threat the virus posed was made quite impossible from the outset. The media and politicians spread a distorted and misleading picture based on fundamental flaws in data collection, mainly as a result of medically incorrect definitions promoted by WHO, the CDC and other health agencies. Each positive laboratory test for the virus was to be reported as a CoViD-19 case, when very often the PCR test was picking up the presence of viral material from previous infections. This definition broke a fundamental first rule of infectiology: the necessity to differentiate between “infection” (invasion and multiplication of an agent in the host) and “infectious disease” (infection with ensuing illness). CoViD-19 is the designation for severe illness that occurs only in about 10% of infected individuals, but because of incorrect designation, the number of so-called ‘cases’ surged.
Another serious mistake was that every deceased person who had tested positive for the virus was recorded in the official records as a coronavirus victim, a method that violated all international medical guidelines. The absurdity of giving CoViD-19 as the cause of death for a terminal cancer patient is an unforgivable fraud that was repeatedly perpetrated on the public during the ‘pandemic’. Correlation does not imply causation, yet this causal fallacy was permitted to drive the world toward catastrophe. The truth pertaining to the virus remained shrouded in rumor, myth, and mistaken belief. A French study, published March 19, 2020, was the first to shed light on the problem. Two cohorts of approximately 8,000 patients with respiratory disease were grouped according to whether they were carrying ordinary everyday coronaviruses like the common cold or SARS-CoV-2. Deaths in each group were registered over two months. However, the number of fatalities did not significantly differ in the two groups and the conclusion followed that the dangers associated with CoViD-19 were probably way overblown. In a subsequent study, the same team compared the mortality rates associated with diagnosis of respiratory viruses during the colder months of 2018–2019 and 2019–2020 in southeastern France. Overall, the proportion of respiratory virus-related deaths among hospitalized patients was not significantly higher for 2019–2020 than the year before. Therefore, the addition of SARS-CoV-2 to the spectrum of viral pathogens did not affect overall mortality rates in patients suffering from respiratory disease.xxii How can any of this be reconciled with the official reports of the horrifying number of CoViD-19 deaths? Two numbers must be known if the danger of viral transmission is to be assessed: the number of infections and the number of deaths.xxiii
Furthermore, it has been determined that the virus is present in the nasopharynx for approximately two weeks, at which point it is possible to detect it. By what means? Viral RNA is transcribed into DNA and quantified by the polymerase chain reaction (PCR). The first assay for the new coronavirus was developed under the guidance of Professor Christian Drosten, Head of the Institute for Virology at the Charité Berlin. This test was used across the world in the first few months of the outbreak. Tests from other laboratories would follow later.xxiv
Diagnostic PCR tests are normally subject to stringent quality assessment and are approved by regulatory agencies before being used. This is important because no laboratory test has ever been found to be 100% correct. Quality control measures were essentially dispensed with in the case of SARS-CoV-2 because an international emergency had been declared. Consequently, nothing was really known about PCR test reliability. In essence, these parameters should give an indication of how many false-positive or false-negative results should be expected. The test protocol from the Drosten laboratory was used worldwide. As it happened, test results played a decisive role in defining political decision-making during the crisis. Yet, data interpretation was often largely a matter of interpretation and belief. What did Drosten himself say on Twitter?
Sure: Towards the end of the illness the PCR is sometimes positive and sometimes negative. Here, chance plays a role. When you test a patient twice as negative and discharge him as cured, it is indeed possible that you can have positive test results again at home. But this is still far from being a re-infection.
Several physician colleagues have informed us of similar haphazard results with patients who had been tested repeatedly during their hospitalization. Is it particularly surprising that goats and papayas tested positive for the virus in Tanzania? The criticism by the President of Tanzania regarding the unreliability of the test kits was of course immediately dismissed by WHO. But today it is perfectly clear that the test result is error-prone, as is every PCR. How much so, and whether there are significant differences among the presently available tests, cannot be determined because of lack of data.
Instead, the Robert Koch Institute (RKI), the German federal government agency and research institute for disease control, stipulated at the beginning that only selective testing should be carried out—exactly the opposite of what should have happened. And as the epidemic ran its course, the RKI stepwise altered the testing strategy—always diametrically in the wrong direction.
At first, only people who had been in high-risk areas or had been in contact with an infected person and also presented with flu-like symptoms were to be tested. At the end of March 2020, the RKI then changed the recommended test criteria to: flu-like symptoms in addition to contact with an infected person. At the beginning of May 2020, the President of the RKI, Professor Lothar Wieler, announced people with even “the slightest symptoms” should be tested.
The responsibility for translating these dubious decisions into action lay entirely within the hands of the local health authorities. An employee at a lab facility was a typical example: the coach of her handball team was coronavirus positive. The players were sent home on a 14-day quarantine order. One player developed symptoms with coughing and hoarseness and wanted to get tested, but was refused on the grounds that she had no fever. A player from a neighboring district had no symptoms but the local health authority ordered a test nevertheless.
This resulted in chaos due to the appalling ineptitude of the authorities from top to bottom. What would have been urgently needed instead were scientifically sound studies to clarify basic issues of virus dissemination. As many as possible should have been tested in outbreak areas. Antibody responses in those that had tested positive could have subsequently been assessed. Only a single such study addressing these questions was undertaken in Germany: the Heinsberg investigation conducted by Professor Hendrik Streeck, Director of the Institute for Virology at the University of Bonn. Aware of the importance of the preliminary data, these were presented at a press conference, where Streeck was ridiculed by the disbelieving media. The fatality rate was dismissed as impossible, as it was ten times lower than what acknowledged experts and WHO had been claiming as established facts. After completion of the study, final results essentially confirming the preliminary report were again presented, and again deemed by the media to be flawed and inconclusive. But the results of the study spoke for themselves and completely contradicted the overhyped propaganda of the media.xxv
How Many Deaths Did SARS-CoV-2 Infections Claim?
Determining how many deaths have resulted from the disease again comes down to the problem of definition: what is a “coronavirus death”? If an individual drives to the hospital to be tested and later suffers a fatal car accident—just as his positive test results are returned—he nevertheless becomes a coronavirus death statistic. If another individual tests positive for CoViD-19 and jumps off the balcony in shock, he also becomes a CoViD-19 death statistic. The same is true for a sudden stroke, etc. As openly admitted by RKI president Wieler, every individual with a positive test result at the time of death is entered into the statistical register. The first “coronavirus death” in the northernmost state of Germany, Schleswig-Holstein, occurred in a palliative ward, where a patient with terminal oesophageal cancer was seeking peace before being dispatched to the “undiscovered country from which no traveler returns.” A swab was taken, just before his demise, which came back positive following his death. He might equally well have tested positive for other viruses such as rhino-, adeno- or influenza virus had he been tested for those.xxvi
However, with the emergence of a new and possibly dangerous infectious disease, autopsies should be undertaken in order to verify the actual cause of death. Only one pathologist ventured to fulfil this task in Germany. Against the specific advice of the RKI, Professor Klaus Püschel, Director of the Institute of Forensic Medicine, Hamburg University, performed autopsies on all “coronavirus victims” and found that not one of those tested had been healthy. Most had suffered from several pre-existing conditions. One in two suffered from coronary heart disease. Other frequent ailments encountered were hypertension, atherosclerosis, obesity, diabetes, cancer, lung and kidney disease, and liver cirrhosis. The same pattern was shown to have occurred in other jurisdictions. Swiss pathologist Professor Alexander Tzankov reported that many victims had suffered from hypertension, most were overweight, two-thirds suffered from heart problems, and one-third were afflicted by diabetes. The Italian Ministry of Health reported that 96% of CoViD-19 hospital deaths had been patients with at least one severe instance of co-morbidity. Almost 50% had three or more pre-existing adverse health conditions.xxvii
Interestingly, Püschel found lung embolisms in every third patient he examined. Pulmonary embolisms usually result from detachment of blood clots in deep veins of the leg that are swept into the lungs. Clots typically form when blood flow is impeded in the legs, as occurs in cases where the elderly spend the day seated and inactive. A high frequency of lung embolisms was already described in deceased influenza patients 50 years ago. Thus, we are not on the verge of discovering a unique aspect of SARS-Cov-2 that heightens its degree of threat, but we nevertheless see worldwide that elderly people are misguidedly responding to the order to stay at home, when the sheer sedentary nature of such shelter-in-place measures endanger their health as much as any virus might. Physical inactivity is a health threat for the elderly in and of itself, thromboses included. Swedish epidemiologist Professor Johann Giesecke recommended exactly the opposite: As much fresh air and activity as possible. It is refreshing to see that some physicians have the courage to speak out and to recommend another regimen.xxviii
While the number of genuine CoViD-19 fatalities remained unknown outside Hamburg, the situation was no better in other countries. Professor Walter Riccardi, adviser to the Italian Ministry of Health, stated in a March 2020 interview with The Telegraph that 88% of the Italian deaths attributed to CoViD-19 actually resulted from other causes. The problem with coronavirus death counts is that the numbers are actually gross overestimates. In Belgium, not only fatalities with a positive CoViD-19 test were entered into the tally, but also cases where CoViD-19 was merely suspected but never verified.xxix
The risk for a person under 65 in Germany was about as high as a daily drive of 24 kilometres. The risk was low even for the elderly over 80 with 10 “coronavirus deaths” per 10,000 Germans over 80. Calculating this number is simple. About 8.5 million citizens are over 80 in Germany, with about 8,500 “coronavirus deaths” recorded in this age group. This leads to an absolute risk of coronavirus death of 10 per 10,000 for the over 80 set. Now realize that every year about 1,200 of 10,000 people over 80 die in Germany (data from the Federal Office of Statistics). Nearly 50% of them due to cardiovascular diseases (CVD), almost one-third from cancer and around 10% (over 100) as a result of respiratory infections. The latter have always been caused by an array of pathogens including those of the coronavirus family. It has become apparent to many medical experts that SARS-CoV-2 is not the “killer virus” the mainstream media has made it out to be.xxx
The WHO estimates that there are approximately 290,000–650,000 flu deaths per year. Now turn to CoViD-19. In May 2020, the RKI calculated that 170,000 infections with 7,000 CoViD-19 deaths equals a 4% case fatality rate, as predicted by WHO. The conclusion to be drawn from these statistics is that CoViD-19 is ten times more dangerous than seasonal flu. However, the number of infections was at least ten times higher because most mild and asymptomatic cases were not properly assessed. This would have brought the number down to a much more realistic fatality rate of 0.4%. Moreover, the number of actual CoViD-19 deaths was lower because many had actually died of other causes. Further correction of the number brings us to a rough estimate of 0.1% – 0.3%, which is in the range of moderate flu. This tallies well with the results of Professor Streeck, who arrived at an estimate of 0.24% – 0.26% for his Hamburg study. The average age of the deceased testing positive for CoViD-19 was around 81 years.
The conclusion that CoViD-19 is comparable to seasonal flu has been reached by many investigators in other countries. In an analysis of several studies, it was shown that, contingent on local factors and statistical methodology, the median infection fatality rate was 0.27%. There are many studies that show that SARS-CoV-2 is a far cry from the “killer virus” it is supposed to be.xxxi Yet, despite this fact, once testing positive for SARS-CoV-2—even falsely for that matter—an individual can remain marked as a CoViD-19 victim for life. Then, irrespective of when and why death occurs, he or she will be entered into the CoViD-19 death register. Thus, the number of coronavirus deaths will continue to soar incessantly, while the War on CoViD like the war on AIDS before it will go on for years until the globalists devise a new obsession to get everyone jittery about.
Fear in the general populace is further fuelled by reports that SARS-CoV-2 is much more dangerous than the flu because it attacks many different organs with probable long-term consequences. Newspaper reports and publications abound that the virus can be found in the heart, liver, and kidneys. It may even find its way to our central nervous system, we are told. Such headlines sound terrifying. However, obtaining positive RT-PCR results for SARS-CoV-2 in organs other than the lung is neither surprising nor significant. Two issues are of decisive importance: the actual viral load and the question of whether the viruses cause any damage. The highest SARS-CoV-2 concentrations have been found in the lungs of patients as one would naturally expect. Traces of the virus have been detected in other organs, which authors Karina Reiss and Sucharit Bhakdi believe is a matter of small concern. Until scientific evidence to the contrary is available, they contend, the findings should be regarded as trivial observations of little to no significance, yet they have been hyped to the max by the press, and the political opportunists that are harnessing the pandemic for their own nefarious purposes.
Is there a great difference between SARS-CoV-2 and the annual flu? Probably in many cases there is not. It has been known for years that influenza can affect the heart and other organs. All respiratory viruses can find their way to the central nervous system. There is no basic difference with SARS-CoV-2.xxxii The fact that SARS-CoV-2 does not constitute a public danger and that the infection often runs its course without symptoms might have one disadvantage. It was originally thought that perhaps asymptomatic people are contagious and unwittingly pass the virus on to others. This fear originated from a publication that reported that the Chinese businesswoman who infected an automotive supplier’s staff member during a visit to Bavaria displayed no symptoms herself. This publication caused a worldwide sensation with expected effects. It was believed that a deadly virus that could be transmitted by healthy individuals must by definition be a swift and invisible killer. This fear became the driving force behind many extreme preventive measures, from visiting bans for hospitalized patients to obligatory mask-wearing. However, in the midst of all the panic and pandemonium, a very important fact was overlooked. The major statement of the publication turned out to be false. A follow-up inquiry revealed that the Chinese woman had been ill during her stay in Germany and was under medication to relieve pain and reduce fever. This was not mentioned in the publication.xxxiii
This shows a general tendency in the media to suppress facts that do not support the dangerous ‘pandemic’ narrative. Why would that be? Call it paranoid if you like, but it looks like the media was tasked with generating as much fear as possible in order to escalate the crisis, with the aim of heightening all the control measures, justifying increased surveillance, tracing and tracking measures, vaccine certificate advocacy, and every other measure that reduced freedom and increased the level of abject serfdom of the population. Does this not accord with a power grab by the global elite? It certainly looks like it.
As for the reaching the verdict that this ‘pandemic’ was planned and that the release of this virus was not accidental the jury is still out. However, when one considers that the military-pharmaceutical-industrial complex is behind the gain-of-function technology that weaponizes viruses by making them more virulent and pathogenic and that the same scientists are behind the effort to develop vaccines to counteract the very viruses they themselves have devised, it is not hard to see that we have as a population have been wedged between a rock and a hard place and are slowly being crushed to death. As for the claim that the virus is a bioweapon released with the purpose of eviscerating certain segments of the population, all that is required is an examination of the effected genomes. There is absolutely no question about the fact that populations with a high ratio of Denisovan and Neanderthal genetics in their genome have been found to be especially vulnerable to the effects of CoViD-19 infection. Does this suggest that such populations have been wilfully targeted by a eugenics program to seek their removal from the human gene pool? That remains to be proven. Hopefully, this paper will have succeeded in opening a can of worms that leads to serious discussion and examination, because it is clear the problem is not going away.
i Jerry Agar, “Pandemic lessons from the 14th century,” The Toronto Star, October 20, 2020.
ii “Spanish Flu killed 50 million and millions more died in war,” The National Post, December 31, 2020.
iii Rachel Schraer, Coronavirus: “Are mutations making it more infectious?” July 1, 2020, https://www.bbc.com/news/health-53325771
iv “Coronavirus mutation may have made it more contagious: study,” by University of Texas, Oct 30, 2020, https://medicalxpress.com/news/2020-10-coronavirus-mutation-contagious.html
v “Machine-learning model finds SARS-COV-2 growing more infectious,” Editorial, August 24, 2020, https://www.ddw-online.com/machine-learning-model-finds-sars-cov-2-growing-more-infectious-3256-202008/
vi “Genetic Mutations Predispose Individuals to Severe COVID-19,” Source: Radboud University, July 26, 2020, https://neurosciencenews.com/coronavirus-genetic-mutations-16705/
vii “Individual genetic variation in immune system may affect severity of COVID-19,” Source: American Society for Microbiology, April 18, 2020, neurosciencenews.com/coronavirus-genetics-immune-system-16199
viii John Hewitt, “Could COVID-19 have wiped out the Neandertals?” December 24, 2020, https://phys.org/news/2020-12-covid-neandertals.html
ix Frank Jordans, “Study: Neanderthal genes are a liability for COVID patients,” September 30, 2020, https://medicalxpress.com/news/2020-09-neanderthal-genes-liability-covid-patients.html.
x Megan Ogilve, Kenyan Wallace and Jennifer Wang, “Shocking Rates Seen in Virus Hotspots: Higher Rate Seen in Lower Income Areas,” The Toronto Star, November 17, 2020.
xi Hugo Zeberg & Svante Pääbo, “The major genetic risk factor for severe COVID-19 is inherited from Neanderthals,” Nature volume 587, pages 610–612 (2020), September 30, 2020, https://www.nature.com/articles/s41586-020-2818-3
xii Zaria Gorvett, “Here’s what we know sex with Neanderthals was like,” Jan 13, 2021,
xiii Joe Pinkstone, “The five genes that make you more likely to die from coronavirus or be admitted to intensive care,” December 11, 2020, https://www.dailymail.co.uk/sciencetech/article-9043703/Five-genes-severe-cases-Covid-19.html
xiv Julia Evangelou Strait, “COVID-19 study looks at genetics of healthy people who develop severe illness: Researchers seek answers to virus’s mysteries, clues to possible treatments,” May 20, 2020, https://medicine.wustl.edu/news/covid-19-study-looks-at-genetics-of-healthy-people-who-develop-severe-illness/
xv Rebecca Morelle, “Covid: Genes hold clues to why some people get severely ill,” Dec. 12, 2020, https://www.bbc.co.uk/news/health-54832563
xvi “Coronavirus: Obesity ‘increases risks from Covid-19,’” August 26, 2020, bbc.com/news/health-53921141
xvii Kate Kelland, “Obesity a driving factor in CoViD-19 deaths, global report finds,” March 4, 2021, ed. Janet Lawrence, https://ca.yahoo.com/news/obesity-driving-factor-covid-19-142725406.html.
xviii Stephanie Seneff, “COVID-19 Reveals a New Metabolism Paradigm,” Foundation for Alternative and Integrative Medicine, originally published in Masters of Health, December 2020, https://www.faim.org/covid-19-reveals-a-new-metabolism-paradigm?fbclid=IwAR0xAzkYfWFyoYaM9ehNTEBd9ygFyrzj-eBihEiVxI8Wlqw2_SZj692KHgI
xix Zaria Gorvett, “The people with hidden immunity against Covid-19,” BBC News, July 2020, https://www.bbc.com/future/article/20200716-the-people-with-hidden-protection-from-covid-19
xx “Coronavirus makes changes that cause cells not to recognize it: Discovery lays groundwork for designing novel antiviral drugs” July 24, 2020, Source: University of Texas Health Science Center at San Antonio, https://www.sciencedaily.com/releases/2020/07/200724104157.htm
xxi The Visual and Data Journalism Team BBC “Covid-19 pandemic: Tracking the global coronavirus outbreak,” December 21, 2020, https://www.bbc.com/news/world-51235105
xxii Dr. Karina Reiss and Sucharit Bhakdi, Corona False Alarm? Facts and Figures, White River Junction, VT: Chelsea Green Publishing, Originally published with Goldegg Verlag GmbH, as Corona Fehlalarm? Friedrichstraße, Berlin, 2020, pp. 11, 12.
xxiii Ibid., p. 12.
xxv Ibid., pp.14,15.
xxvi Ibid., pp.15, 16.
xxvii Ibid. p.16.
xxviii Ibid., pp.16, 17.
xxix Ibid., p.17.
xxxi Ibid., pp.19, 20.
xxxii Ibid., p.21.
xxxiii Ibid., p.22.