Burden of Proof: Deconstructing Arguments and Evidence on the Origins of SARS-CoV-2.

“In questions of science, the authority of a thousand is not worth the humble reasoning of a single individual” Galileo Galilei

Disclaimer: As a non-scientist I recognize my limitations in the understanding and interpretation of the detailed, highly specialized and complex scientific terminology and data in the papers critiqued.

Preamble:
The scientific process is well documented, and involves making observations, raising questions from what is observed, forming hypotheses, making predictions based on those hypotheses, testing the predictions, and using the findings to make new hypotheses or raise further questions for investigation. Leaving aside professional research, scientists in industry, academics and their students in universities, this process is not widely discussed or understood in the public domain. Moreover, the scientific papers written on SARS-CoV-2 use a language beyond the grasp of non-scientists and the layperson. I am not a scientist, so in deconstructing the arguments and evidence presented by Anderson, Rambaut, Lipkin, Holmes, & Garry (2020), Sirotkin & Sirotkin (2020) and Segreto & Deigin (2020) I have on occasion used metaphors, similes and analogies in an attempt to create an understanding of the importance of their work. Moreover, I wanted to gain insight and knowledge to questions which have been by and large dismissed by politicians, some scientists and not fully investigated by the media. In doing so, I am seeking knowledge and understanding into the greatest health crisis to befall humanity in our lifetime. I approach the data with an open mind, with no desire to promote any fixed concept or seek to engender controversy for its own sake.


Introduction
“Might SARS-CoV-2 have arisen via serial passage through an animal host or cell cultures” (Sirotkin & Sirotkin, 2020) is the hypothesis which forms the basis of an argument on the origins of SARS-CoV-2.
Studies into the genetic structure of SARS-CoV-2 posit a similar inquiry “The genetic structure of SARS-CoV-2 does not rule out a laboratory origin” (Segreto & Deigin, 2020).
While hedging a bet may also be a valid hypothesis: “The proximal origin of SARS-CoV-2” (Anderson, Rambaut, Lipkin, Holmes, & Garry, 2020)
Posing a question, and following it up with extrapolations based on historical antecedents isn’t spreading a conspiracy theory. It is science at work in the real world we inhabit. Seeking answers through the scientific method recognizes that science far from being an ideology with a political agenda, is a rigorous discipline which allows other scientists to conduct further research, so that hypotheses are better understood, and proven as fact or rejected through a lack of evidence.
Sirotkin & Sirotkin:
The question of the origins of SARS-CoV-2 is the premise upon which Sirotkin & Sirotkin (2020) formulate their argument. They acknowledge from the outset that their peers in the scientific community have reached the conclusion that the virus causing the current pandemic has not been created or engineered in a laboratory; but, rather is the result of natural infectivity across species. Sirotkin & Sirotkin argue that this conclusion fails to consider two unique genomic features only found in SARS-CoV-2. These genetic qualities are found in the spike protein of the virus. The first one is noted in the receptor binding domain (RBD) of the spike protein which allows the virus to fuse with our cells. This is 3rd on the right in Fig.1 below and looks like a painting done by an elephant’s tail:

Fig1 (Thomas, 2020)

Our cells are tiny living entities. They are protected by an outer layer called a plasma membrane. This layer has two functions. Firstly, it separates the interior of the cell and its working life, from all the activity occurring around its exterior. Secondly, the exterior is able to communicate via a receptor (see Fig 1.) with visitors who may wish to enter its interior for either good or ill intent. SARS-CoV-2 is a visitor with ill intent. Its Trojan-like behavior signals to our cell surface that it wishes to enter. It then invades and replicates itself throughout our body. Sirotkin & Sirotkin note that the receptor binding domain of SARS-CoV-2 has taken a greater liking to the surface membrane of our cells rather more quickly than other SARS like viruses, and over a shorter period of time (Sirotkin & Sirotkin, 2020).
This may have happened naturally, or through a scientific process called gain of function research. The gain of function process is used in virus research to manipulate a virus and mimic its natural interspecies infectivity jump. Generally, this kind of research is used to understand virus behavior, and to develop vaccines to mitigate the kind of global health crisis we are struggling with due to the SARS-CoV-2 pandemic. However, it is also used to develop bio-weapons (Sirotkin & Sirotkin, 2020).
The second observation Sirotkin & Sirotkin (2020) note about the SARS-CoV-2 spike protein is in its unique genetic configuration. It shows a Furin cleavage site (not as warm and fuzzy as it sounds- see 2nd illustration Fig.2). It consists of a unique combination of multiple basic amino acids, not found in SARS-CoV or its other relational viruses:

Fig.2 (Örd, Faustova, & Loog, 2020)

Sirotkin & Sirotkin (2020) claim that this unique feature of the SARS-CoV-2 spike protein is a fusion of avian influenza virus and Newcastle disease virus proteins that have been manipulated under laboratory conditions, or isolated from commercial animal farm environments. The commercial animal farm environment mimics the laboratory conditions of gain of function research practices (Sirotkin & Sirotkin, 2020). Further they assert no influenza virus with a Furin cleavage site has ever been found in the natural world. Those found on commercial farms environments which create the kind of quasi-natural conditions which produce a Furin cleavage site, or those created through gain of function manipulation in a laboratory are highly pathogenic and are able to establish “systemic multi-organ infections” in humans. (Sirotkin & Sirotkin, 2020).
SARS-Cov-2 is the only coronavirus in its ancestry showing a full Furin cleavage site (see Fig.2). Laboratory experiments have shown that Furin cleavage sites within influenza viruses, specifically the avian flu virus and the Newcastle virus, cause lymphopenia in mice, and brain disorders in ferrets. Similar manifestations of these diseases have been recorded in the clinical observations in hospitalized patients infected by SARS-CoV-2, and suffering from COVID-19 (Sirotkin & Sirotkin, 2020).
They postulate that the Furin cleavage site in SARS-CoV-2 may also be an example of the independent evolution that directs virus-host mutagenesis over different periods of time. This process might explain the diverse pathogenic bio-physical reactions between SARS-CoV-2 and its host, the human body. Moreover, they argue that given the historical antecedents of biological research in which viruses are manipulated in a laboratory either through live cultures or through live animals, it is inconceivable not to consider both scenarios for the origins of SARS-CoV-2; either a laboratory leak, or infectivity through a natural jump across species (Sirotkin & Sirotkin, 2020).
To further their argument on the origins of SARS-CoV-2, Sirotkin & Sirotkin (2020) give details of historical antecedents on gain of function research in laboratories, and evidence of leaks and accidents where a virus has inadvertently contaminated a site or parts of a population. According to the authors, the 1977 Russian flu pandemic was caused by a strain of H1N1 Swine flu (A/USSR/90/77), a variant of the 1918 flu virus which caused the pandemic. The H1N1 variant was subject to laboratory manipulation, and it either leaked out of a Soviet Union laboratory, or was introduced into the population through a controlled vaccine trial in 1977. The authors claim that no-one has taken responsibility for the emergence of this virus out of a laboratory. According to Sirotkin & Sirotkin (2020), due to its unique genetic structure and its inexplicable distance from its lineage, it was at the time, the first known example of a virus created through gain of function processes, and escaping out of a biological research center. One noteworthy point the authors make is that viruses manipulated in a laboratory artificially boost genetic divergence between the virus lineages. This results in the accrual of genetic distance at a quicker pace than would occur in the natural world (Sirotkin & Sirotkin, 2020).
Two years after the release of a genetically altered H1N1 Swine flu into the population, another laboratory in the Soviet Union leaked weaponized anthrax out of its bio-weapon laboratory through faulty exhaust fans (Sirotkin & Sirotkin, 2020). Sixty four people were killed. Initially covered up and blamed on contaminated meat the victims ate, it took 20 years for the truth to be revealed. The point the authors make is twofold; firstly there is a history of denying laboratory leaks, and secondly, not all gain of function research is a humane endeavor (Sirotkin & Sirotkin, 2020).
Genetic manipulation of viruses has continued for decades, albeit with little debate by public intellectuals or even the mainstream media itself. In 2011 serial passage and gain of function research was able to create an aerosol based, lethal and highly transmissible influenza virus by infecting ferrets with the deadly H5N1 bird flu (Sirotkin & Sirotkin, 2020). According to the authors, a reporter noted that “this highly virulent strain would make the deadly 1918 flu pandemic look like a pesky cold” (Sirotkin & Sirotkin, 2020). More disturbing experiments on animals followed. A scientist from the Universities of Tokyo and Wisconsin combined the genetic code of H1N1 Swine flu and H5N1 bird flu to generate a chimeric virus which was injected into ferrets. This experiment produced another deadly airborne virus with pandemic potential.
A continuation of gain of function and serial passage research combining H7N1 Bird Flu with ferrets, and H1N1 Bird Flu with swine, increased the infectiousness of these viruses. Moreover, and most noteworthy, these viruses produced the highly contentious and somewhat mysterious Furin cleavage site in their spike protein, which is also found in SARS-CoV-2. As previously noted Furin cleavage sites only appear in the spike protein after serial passage in a laboratory, or a quasi-natural symbiotic process on commercial animal farms.
A key point the authors note about these experiments is that the direct genetic engineering of these viruses through a combined modified genome sequence, leaves little evidence of artificial design. The viruses appear as if they are the result of a rapid cross species infectivity process in the natural world (Sirotkin & Sirotkin, 2020).
Gain of function experiments in a laboratory edit a long time lapsed natural phenomenon into a small temporal window. But, under intense analysis, some very subtle differences may be found in the genetically engineered viruses. However, it is necessary to unlock the unexplained genetic distance from its lineage to fully understand the evolutionary history of the virus. Sirotkin & Sirotkin (2020) assert that mutations of SARS-CoV-2 could have occurred in an intermediary natural host, or via a gain of function process, or through laboratory based serial passage. Thus explaining the SARS-CoV-2 spike protein binding to human AEC2 “some 10-20 times higher than other coronaviruses” (Sirotkin & Sirotkin, 2020). SARS-COV-2 adapted quickly to humans at the start of the pandemic, whereas SARS-CoV in 2002-4 was in its final stage of adaptation as it spread more rapidly through populations. Viruses generally mutate over time before they adapt to a new species (Sirotkin & Sirotkin, 2020).
The Mysterious Furin Cleavage site in SARS-CoV-2 (Sirotkin & Sirotkin):
Ferrets have been purposely infected with genetically modified influenza viruses which contain a Furin cleavage site due to a couple of molecular processes, 1) “nucleotide insertions through serial passage processes, and 2) the recombination of multiple viral nucleic acids inside a host cell. The latter could have included additional viruses introduced through accidental laboratory co-infections” (Sirotkin & Sirotkin, 2020). However, ferrets haven’t been purposely infected with any lineage of the coronavirus family, so there must be another explanation for the presence of the Furin cleavage site in several types of coronavirus.
Sirotkin & Sirotkin (2020) argue that a molecular pathway or foot print must exist. The evidence they cite is three fold. Firstly, it is possible this occurs through laboratory based serial passage research and the symbiotic relationship between virus and host cells. Secondly they note that when chickens were infected with a lethal bronchitis coronavirus (IBV) the virus developed significant mutations along its spike protein, and inflicted substantial lethality, including neural damage not previously seen in the IBV coronavirus. It also ravaged the respiratory and urinary systems in the same manner that SARS-CoV-2 perpetrates on the multi-organs of human beings, including the lungs, cardiovascular system, nervous system and kidneys (Sirotkin & Sirotkin, 2020). Thirdly, a coronavirus found in cattle was extracted and genetically modified generating a Furin cleavage site in a small sample of the pooled viruses. This modified virus, due to its spike protein, became the dominant strain (Sirotkin & Sirotkin, 2020).
Unlike other coronaviruses in its lineage, the resourcefulness and cleverness of SARS-CoV-2 to acquire the Furin cleavage site, enables the virus to spread rapidly and with ease throughout the human population. There are only three possible ways for SARS-CoV-2 to obtain a Furin cleavage site. Firstly, through a natural recombination via a secondary host in the wild. Secondly, through serial passage research in a laboratory, or quasi-naturally on a commercial animal farm. Thirdly, and more contentiously, the purposeful genetic modification of the virus in a laboratory using a well-known recombinant DNA technology, which has been in use for over twenty years. According to the authors this kind of deconstruction and reconstruction of the virus using this technology, creates a virus without obvious evidence of manipulation (Sirotkin & Sirotkin, 2020).
The counter argument against Sirotkin & Sirotkin’s (2020) third example is that notwithstanding SARS-CoV-2’s high affinity for the human enzyme ACE2; engineering a Furin cleavage site nucleotide by nucleotide is not possible. However, in response to this criticism they argue that it could very well have occurred after serial passage processes through ferrets, or in the cell cultures of a laboratory. Moreover, in the absence of hard evidence for the purposeful creation of the whole receptor binding domain of the SARS-Cov-2 spike protein sequence, there are not any genetic data to differentiate between a natural and engineered SARS-CoV-2, unless proven otherwise (Sirotkin & Sirotkin, 2020).
Segreto & Deigin:
“The genetic structure of SARS-CoV-2 does not rule out a laboratory origin” is the hypothesis put forward by Segreto & Deigin (2020). While citing similar evidence to Sirotkin & Sirotkin (2020); Segreto & Deigin (2020) assert that it is less likely that the virus occurred naturally, or through cell/animal serial passage. It is more likely to be the direct result of laboratory gene mutation (Segreto & Deigin, 2020). They describe how the two unique features in SARS-CoV-2; the Furin cleavage site and the lethal receptor binding domain may have been acquired rapidly, and more or less at the same time. Such a fast mutation of the virus is unlikely to have occurred through natural cross infectivity between animal species, then into humans.
Scientists from the Wuhan Institute of Virology (WIV) were the first people to classify and differentiate SARS-CoV-2 from other SARS-CoV which caused an epidemic in 2002-4. The closest relatives to SARS-CoV-2 are bat and pangolin coronaviruses. A covid DNA sequence from a bat (Rhinolophus affinis) is the nearest evolutionary family member to SARS-CoV-2. Segreto & Deigin (2020) note that its genome sequence mapping was not released publicly before the outbreak of the SARS-CoV-2 pandemic, despite collecting the virus sample in Yunnan province (China) in 2013. (Segreto & Deigin, 2020).
Six miners from Yunnan province had contracted a severe pneumonia in 2012. Three died. Researchers from WIV investigated the mine and found that contracting the serious illness correlated with the time span the miners spent in the cave clearing out bat excrement. (Segreto & Deigin, 2020). The surviving miners underwent tests and were found to have developed antibodies for SARS. According to Segreto & Deigin (2020), it is unlikely that the miners retained antibodies for 10 years from the 2002-4 SARS epidemic. They suggest that an antibody test given to the miners may have cross reacted with a novel SARS like bat virus the miners contracted while working in the cave (Segreto & Deigin, 2020).
The second covid DNA sequence closest to the bat mentioned above was found in a pangolin in 2019. This animal was trafficked illegally from Malaysia to Guangdong province in China. The envelope protein (the outermost layer of the virus) of the pangolin was found to have a 100% match with the amino acids of the bat’s envelope protein. These matching envelope proteins were found in some of the early DNA sequencing of SARS-CoV-2.
It has long been speculated that pangolins could have been the intermediary host for cross infectivity of SARS-CoV-2 into humans. The genome sequencing of the pangolin’s RBD in its spike protein, while lower than the bat, was found to be almost identical to SARS-CoV-2. Segreto & Deigin (2020) note that the pangolin coronavirus has matching amino acids at five critical junctures in its spike protein receptor binding domain as SARS-CoV-2, whereas the bat only shares one amino acid with SARS-CoV-2. The authors also note that the human angiotensin converting enzyme (ACE2) sequence is found to be higher between pangolins and humans, than between bats and humans. Further they claim that studies of the receptor binding domain of the bat indicate that it does not bind with pangolin ACE2. But, the spike protein of SARS-CoV-2 has a greater attraction to human ACE2 receptor, than to those of pangolins and bats (Segreto & Deigin, 2020). This is similar to the findings of Sirotkin & Sirotkin (2020).
Segreto & Deigin (2020) acknowledge that the fusion of the spike proteins of pangolins and bats could have occurred via natural cross species infectivity to create a chimeric virus: SARS-CoV-2. For this to happen, the two viruses would have to infect the same cell in the two organisms of the animals, at the same time. They argue that given the low population density of pangolins, and the scarce presence of coronaviruses in the natural population of pangolins, this is an unlikely scenario (Segreto & Deigin, 2020).

The Mysterious Furin Cleavage site in SARS-CoV-2 (Segreto & Deigin)
The genome sequence of SARS-CoV-2 is different from its closest bat relative. The most significant distinction is in the spike protein of SARS-CoV-2. In SARS-CoV-2 there is a Furin cleavage site that has been generated by a host cell Furin enzyme. Furin is a protein that is encoded with the Furin gene. The Furin gene communicates with the Furin protein to activate itself. This activation causes the Furin protein to cleave or split (Segreto & Deigin, 2020). But the process isn’t linear, it is more like a tiny, miniscule big bang. The amino acids reorganize themselves into their own DNA inspired cellular universe. In doing so they create their own unique molecular footprint; one that is out of step with the rest of its cellular structure, and not anything like the genome sequence of the spike proteins found in other coronaviruses.
This cellular chemical reaction has not been seen in other bat and rodent coronaviruses, nor the Middle East Respiratory Syndrome (MERS) coronavirus (Segreto & Deigin, 2020). The molecular footprint of the Furin site in SARS-CoV-2 does not match the molecular footprint of any of its closest relative coronaviruses. It remains distinctive in this regard (Segreto & Deigin, 2020). So, the questions are: did the Furin cleavage site in SAR-CoV-2 evolve naturally through a mutation process during its DNA replication? Or was it due to recombination through artificially joining segments of the SARS-CoV-2 DNA from different animal host cells?
Segreto & Deigin (2020), argue that given the two decades of research on bat SARS-Covs; justified through the assumption that they could jump naturally from animals to humans; the artificial design and subsequent leak or escape from a laboratory of SARS-CoV-2 is a plausible theory. They also raise concerns about the modification and deletion of the Wuhan Institute of Virology’s viral database. They suggest that access to over 60Mb of data could help fill in the gaps required to understand the origins of SARS-CoV-2 (Segreto & Deigin, 2020).

Anderson, Rambaut, Lipkin, Holmes, & Garry:
Anderson, Rambaut, Lipkin, Holmes, & Garry (2020), argue that it is possible that the SARS-CoV-2 spike protein acquired its mutations in a laboratory based cell culture, but unlikely. Researchers would have had to use a reverse genetic technique from laboratory stored coronaviruses, and genetically altered the cell’s backbone or molecules (Anderson, Rambaut, Lipkin, Holmes, & Garry, 2020). They argue that the genetic data on SARS-CoV-2 shows “irrefutably that SARS-CoV-2 is not derived from any previously used backbone” (Anderson, Rambaut, Lipkin, Holmes, & Garry, 2020). In addition, the elevated capacity of the SARS-CoV-2 spike protein to bind with human ACE2 could not have been foreseen by simulations which tested the receptor binding domain of the SARS-CoV viruses (Anderson, Rambaut, Lipkin, Holmes, & Garry, 2020). However, new models based upon the analysis of the amino acids in the receptor binding domain of the spike proteins of SARS-CoV like viruses are better able to forecast how they adapt more easily to human ACE2 (Anderson, Rambaut, Lipkin, Holmes, & Garry, 2020). In particular, the genetic material of a SARS like bat coronavirus (BatCoV Rs 3367) shares nearly a 100% identity with a bat virus (WIV1) which causes severe acute respiratory syndrome. BatCoV Rs 3367 shares four of the six protein reactive chemicals present in the spike protein of SARS-CoV-2. Therefore the assumption is that bats could be the original hosts for the ancestors of the virus SARS-CoV-2. But further sampling of bats and other animals which carry coronaviruses is required to correctly identify its historical lineages. (Anderson, Rambaut, Lipkin, Holmes, & Garry, 2020). The spike protein of CoV chimeric strains of a bat-like coronavirus (those created through laboratory design) may attach to human ACE2 with more flexibility than previously envisaged. This explains why SARS-CoV-2 has been able to adapt, and bind efficiently with human ACE2 (Anderson, Rambaut, Lipkin, Holmes, & Garry, 2020).
The finding of SARS-CoV like viruses in pangolins, which have an approximate indistinguishable spike protein from SARS-CoV-2, could explain the cross species infectivity and the leap into humans (Anderson, Rambaut, Lipkin, Holmes, & Garry, 2020). The SARS-CoV-2 spike protein’s omnivorous appetite for ACE2 extends beyond humans to cats and ferrets also. This they claim is the result of natural selection, and is stronger evidence than an argument of purposeful manipulation (Anderson, Rambaut, Lipkin, Holmes, & Garry, 2020). Additional research may solve the mystery of the Furin cleavage site in the spike protein of SARS-CoV-2. It could be discovered in other species that do not have a direct link to SARS-CoV viruses, but are related to a wider coronavirus genus. Perhaps SARS-CoV-2 was spreading asymptomatically throughout communities in Wuhan, before serious infections and illness arose. This could explain how over an as yet undetermined period of time, SARS-CoV-2 acquired its high affinity to human ACE2, and its ability to infect multiple organs in the human body (Anderson, Rambaut, Lipkin, Holmes, & Garry, 2020).
Sirotkin & Sirotkin (2020) claim that it is possible to genetically manipulate the molecules of a cell without leaving a trace. Segreto & Deigin (2020) argue that the bat-pangolin-human cross species infectivity hypothesis is questionable due to “the accuracy of their assembly data” (Segreto & Deigin, 2020). In other words errors have been found in the analysis of the genetic data used to put forward this theory. Segreto & Deigin (2020) also argue that research based experiments on a bat coronavirus (RaTG13), demonstrate that it is unable to bind to the ACE2 in horseshoe bats, whereas SARS-CoV-2 is able to do so. Moreover, while bat coronavirus RaTG13 is able to bind to human ACE2, it doesn’t do so well with the ACE2 of rats and mice. SARS-CoV-2 did not bind at all with the ACE2 of rats and mice (Segreto & Deigin, 2020). This, they argue, refutes the claim by Anderson, Rambaut, Lipkin, Holmes, & Garry (2020) that bat coronaviruses are the likely ancestors of SARS-CoV-2.
Conclusion:
Sirotkin & Sirotkin (2020), Segreto & Deigin, (2020), and Anderson, Rambaut, Lipkin, Holmes, & Garry, (2020) use historical evidence, scientific data and recorded experiments to form their hypothesis on the origins of SARS-CoV-2. For example, a life-threatening virus is causing suffering and death across the world. There is no conclusive evidence of its origins. There are examples of the genetic modification of viruses in laboratories, the escape of a virus from a laboratory, and the quasi-natural development of similar viruses on commercial animal farms. There’s an evidence based relationship between SARS-CoV-2 like viruses with similar spike proteins in other animals in the wild. Further, the Centre for Arms Control and Proliferation warns of a one in four chance of a virus leak from a laboratory (Sirotkin & Sirotkin, 2020).
While investigating and analyzing similar data, Sirotkin & Sirotkin (2020), Segreto & Deigin, (2020), and Anderson, Rambaut, Lipkin, Holmes, & Garry, (2020) reach different and often dissenting conclusions. However, their use of persuasive evidence to explain the molecular footprint and DNA genome sequencing of SARS-CoV-2, SARS-CoV, and other relational coronaviruses and influenza viruses, sustains the scientific evidence required for burden of proof. All agree that until such time more scientific data are gathered, and more unrestricted access to the location where the disease is thought to have emerged is granted; the root cause of SARS-CoV-2 is irresolvable. It is not possible to disprove each other’s arguments on the origins of SARS-CoV-2.
Sirotkin & Sirotkin (2020), Segreto & Deigin, (2020), and Anderson, Rambaut, Lipkin, Holmes, & Garry, (2020) present compelling evidence; but, is it enough to meet the burden of proof?
Day-to day burden of proof relies on common sense. “I have contracted Covid-19” is easy to prove as my signs and symptoms, along with a positive PCR test indicate the presence of SARS-CoV-2 in my body. I have met the conditions for the burden of proof. If I argue that SARS-CoV-2 came from aliens, then this is an erroneous argument. There is no evidence that aliens exist. If I claim scientists created SARS-CoV-2 in a laboratory in China and it leaked out or escaped by unknown means, and have no evidence for the assertion; it is an erroneous claim. Similarly, if I assert that SARS-CoV-2 was first circulating in the United States of America, and provide no evidence; it is an erroneous claim.
If I form a hypothesis like “Might SARS-CoV-2 Have Arisen via Serial Passage through an Animal Host or Cell” (Sirotkin & Sirotkin, 2020) , or “The genetic structure of SARS-CoV-2 does not rule out laboratory origin” (Segreto & Deigin, 2020), or “The proximal origin of SARS-CoV-2” (Anderson, Rambaut, Lipkin, Holmes, & Garry, 2020) burden of proof of the hypotheses are required for the claim to be valid. In the arguments of Sirotkin & Sirotkin (2020), Segreto & Deigin, (2020), and Anderson, Rambaut, Lipkin, Holmes, & Garry, (2020), the verification of the scientific evidence they cite is similar, while the conclusions drawn from similar data are different. Overall their collective evidence arbitrates between their competing hypotheses, and provides the burden of proof in seeking the origins of a global pandemic caused by SARS-CoV-2. A pandemic that is causing millions of deaths, and unbearable suffering and heartbreak to millions of people around the world.

References:
Anderson, K., Rambaut, A., Lipkin, I. W., Holmes, E. C., & Garry, R. F. (2020). The proximal origin of SARS-CoV-2. Nature Medicine, 26, 450-452.
Örd, ,. M., Faustova, l. l., & Loog, M. (2020, October 9). The sequence at Spike S1/S2 site enables cleavage by Furin and phospho-regulation in SARS-CoV2 but not in SARS-CoV1 or MERS-CoV. Retrieved from Scientific Reports, No 10, 16944: https://www.nature.com/articles/s41598-020-74101-0
Segreto, R., & Deigin, Y. (2020). The genetic structure of SARS-CoV-2 does not rule out a laboratory origin. BioEssays, 1-9.
Sirotkin, K., & Sirotkin, D. (2020). Might SARS-CoV-2 Have Arisen via Serial Passage through an Animal Host or Cell Culture. BioEssays, 1-7.
Thomas, L. (2020, June 8). The receptor binding domain of the SARS-CoV-2. Retrieved from News Medical Life Sciences: https://www.news-medical.net/news/20200608/The-receptor-binding-domain-of-the-SARS-CoV-2.aspx

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