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  • What is the likelihood that coronavirus was made in a lab?

    Avatar IveyTech updated 3 days, 23 hours ago 3 Members · 6 Posts
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    mhadfield

    Administrator
    April 9, 2021 at 1:48 pm
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    ArchipeligoLeach

    Member
    April 12, 2021 at 4:38 am

    I think the simpler question is what is the likelihood that COVID-19 escaped from a lab? You don’t need to include the question of deliberate human manipulation of the virus. The Chinese Communist Party is doing everything they can to suppress and hide any possible evidence the virus was released from the Wuhan Lab. They demanded approval of the people the WHO sent over to investigate. They greatly constrained the scope of the investigation, blocking the ability to investigate anything in the Wuhan labs. So no surprise that the official conclusion of this sham investigation is that there is no evidence for a lab release. It’s like saying that during World War II before the Allied invasion of Germany there was no evidence of massive Nazi extermination campaigns. Knowing the effort the CCP has taken to shield the Wuhan Lab, any person with common sense would have to conclude that that is the likely source.

    Remember, this is the same CCP that put incredibly strict restrictions on travel within China to curb the spread of COVID-19 within China. But at the same time they deliberately promoted travel between the Wuhan region and the rest of the world, accusing anyone trying to restrict this travel as being racist or xenophobic. They wanted to spread this virus far and wide throughout the world. It is the first successful global biological warfare attack in the history of man. That is even more damning than an accidental release from the Wuhan lab.

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    IveyTech

    Member
    April 14, 2021 at 2:59 pm

    “The most pronounced difference between SARS-S and SARS-2-S is an additional furin cleavage site (site 1, Figure 2A) resulting from an insertion of 12 nt at the boundary between S1 and S2 [8,11,29]. This additional furin cleavage site is shared among all sequenced SARS-CoV-2 genomes, but absent in all their closest known relatives such as bat RaTG13 and those isolated from pangolin [29]. The seemingly sudden appearance of this additional polybasic furin cleavage site 1 has been a lasting source of conspiracy theory that SARS-CoV-2 is man-made, which is discussed later.”

    “…The furin cleavage site was predicted in February 2020 [8] and, in May 2020, its functional importance was confirmed, i.e., that the cleavage was essential for efficient viral entry into human lung cells[…]”

    “…In addition to site 1 and site 2 (Figure 2A) that cleave SARS-2-S into the S1 and S2 domains, a third cleavage site also exists for cleaving S2 into FP and S2′ domains (Figure 2B,D). This site, often referred to as the S2′ site, is likely cleaved by TMPRSS2 [41,42,43,44], consistent with the finding that TMPRSS2 is needed for SARS-CoV-2 infection[…]”

    “As previously mentioned, the additional polybasic furin cleavage site 1 (Figure 2A) has been a lasting source of conspiracy theory that SARS-CoV-2 is man-made. Advocates of the conspiracy theory assume that scientists have ignored or refused to address their legit concerns[…]”

    “…First, the furin cleavage site has not been observed in any close relatives of SARS-CoV-2 in nature. A somewhat similar furin cleavage site was present at a roughly homologous site in S protein of the murine hepatitis virus [45] and in a few alphacoronaviruses [2,8,29]. However, it is not clear how SARS-CoV-2 could gain it from these remote relatives. While recombination might be a possibility, there is hardly any sequence homology between SARS-2-S and its homologues in the murine hepatitis virus or alphacoronaviruses at sequences flanking the cleavage site, therefore, a recombination origin of the cleavage site is tenuous at present. An insertion at the same site was found in a bat-derived coronavirus [92], but the inserted sequence was different and could not function as a furin cleavage site. A novel bat-derived coronavirus (RmYN02) was reported to have an insertion bearing a weak semblance to the polybasic furin cleavage site in Figure 2A [92], suggesting the possibility of a natural origin of the polybasic furin cleavage site. However, the sequence homology between RmYN02 and SARS-2-S is low, and it is not clear if the insertion in RmYN02 is real or an artefact of alignment. Therefore, if one cannot offer a plausible hypothesis of natural origin of the polybasic site, it is easy to fall back on the hypothesis of artificial origin. This reminds us of the period of time before Darwin, i.e., when the origin of species cannot be fully explained, it is easy to fall back to the theory of a creator.

    The second reason for the conspiracy theory is associated with the feasibility of creating such a polybasic site and a need to create such a site for testing certain biological hypotheses. Some background information arising from SARS-S is needed to understand this reason. The roughly homologous RNA segment in SARS-S is a weak cleavage site, likely cleaved by transmembrane serine protease TMPRSS2 [93]. R667 in SARS-S (immediately upstream of the site 1 cleavage in Figure 2A) is required for cleavage by TMPRSS2 [93]. The site can also be cleaved by trypsin, and processing of SARS-S by trypsin enhances viral infectivity [34,45,94]. Because trypsin and trypsin-like proteases are strongly tissue restricted (Figure 2C), the site is typically not cleaved in SARS-S [24]. It is natural for one to hypothesize that adding a furin cleavage site would allow the site to be efficiently cleaved in nearly all tissues, potentially enhancing SARS-CoV infection and broadening its cell tropism. Indeed, introducing a furin cleavage site at the S1 and S2 boundary of SARS-S has increased cell-cell fusion (syncytium formation) and viral infectivity [34]. This result suggests that the additional polybasic furin cleavage site may have contributed significantly to the efficiency of SARS-CoV-2 in infecting human. Host cells, in response to viral infection, may reduce furin activities [8].

    In short, given the seemingly sudden appearance of the additional furin cleavage site that cannot be readily explained by a hypothesis of natural origin, and the fact that virologists have already experimented with adding a furin cleavage site at this specific location and learned the consequence of enhanced viral infectivity and cell-cell fusion, the claim that the polybasic furin cleavage site in SARS-2-S has been experimentally inserted is not too far-fetched. However, the global collaboration among scientists, in general, and virologists, in particular, has created scientific communities that are far more closely knit than before. While it is possible to create a viral pathogen, it is extremely unlikely for a laboratory to create SARS-CoV-2 without being noticed.

    The third reason is that the 12 nt insertion encoding the polybasic furin cleavage site carries two CpG dinucleotides. Such CpG dinucleotides are very rare in SARS-CoV-2 [95], and particularly rare in SARS-2-S. Why would such CpG rarity contribute to the conspiracy theory? Mammalian zinc finger antiviral protein (ZAP, gene name ZC3HAC1) targets CpG dinucleotides in viral RNA to mediate RNA degradation and inhibit viral replication [96]. The ZAP-mediated RNA degradation is cumulative [96], as shown by the following experiment. When CpG dinucleotides were experimentally added to individual viral segment 1 or 2, the inhibitory effect of ZAP was weak. However, when the same CpG dinucleotides were added to both segments 1 and 2, the ZAP inhibition effect was strong [96]. This implies that only mRNA sequences of sufficient length would be targeted by ZAP (i.e., S, 1ab, and 1a mRNAs in SARS-CoV and SARS-CoV-2). SARS-CoV-2 and its closest relatives from bat (RaTG13) and pangolin exhibit the strongest genomic CpG deficiency among all betacoronaviruses [95], presumably to evade ZAP-mediated host defense. The S gene is particularly CpG-deficient as measured by two indices, I<sub>CpG</sub> [95,97] and ln (N<sub>CG</sub>/N<sub>GC</sub>) (Table 1), where N<sub>CG</sub> and N<sub>GC</sub> are the numbers of CpG and GpC dinucleotides in the S gene. I<sub>CpG</sub> < 1, or ln (N<sub>CG</sub>/N<sub>GC</sub>) < 0, means CpG deficiency.

    Table 1

    Genomic CpG deficiency in the coding sequence encoding the spike proteins, measured by two indices: I<sub>CpG</sub> = (P<sub>C</sub>*P<sub>G</sub>/P<sub>CG</sub>) and ln (N<sub>CG</sub>/N<sub>GC</sub>). The expectation of no CpG deficiency is 1 for I<sub>CpG</sub> and 0 for ln (N<sub>CG</sub>/N<sub>GC</sub>).

    Because of this ZAP-mediated selection against CpG, SARS-CoV-2 and its close relatives encode most of arginine residues by the two AGR codons, instead of the four CGN codons. The S gene encodes 42 arginine residues, with only 12 (28.57%) encoded by the four CGN codons in contrast to 30 encoded by the two AGR codons. The two arginine residues in the polybasic furin cleavage site are encoded by the rare CGN codons, which seems unnatural in this context. However, the probability of randomly picking up two arginine codons that happen to be both CGN codons is not extremely low (i.e. =0.2857<sup>2</sup> = 0.0816).

    One way to dispel the conspiracy theory is to find a set of viral lineages in wildlife that would allow reconstruction of a plausible evolutionary path leading to the origin of the polybasic furin cleavage site[…]

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7829931/#!po=43.9597

    (See the source at the discussion about “Is Moderna vaccine safe in the long term” as it pertains to vaccines)

    – – – – – –

    Also there is a “war” of research virologists/immunologists amongst themselves about what the RaTG13 written genome sequence really is (no actual sample exists?). The furin cleavage site is a point of disagreement whether it is a “smoking gun” pointing towards artificial mutation, also known as “gain-of-function” of a virus. Why would a virus have the evolutionary intelligence to jump species being that it has no classic “desire” to survive nor produce offspring for its posterity? Move a few letters, add a few letters of DNA…but what designed and foresaw the virus’ survival? “P-o-s-t-e-r-i-t-y” becomes “preposterous” by shifting your point of view and also by moving/changing/adding/subtracting the building blocks (letters).

    Q. So how about a lab scientist deliberately moving DNA building blocks around…if you can see the analogy.

    The link to https://mobile.twitter.com/DrLiMengYAN1?ref_src=twsrc%5Etfw%7Ctwcamp%5Etweetembed%7Ctwterm%5E1379813194156408837%7Ctwgr%5E%7Ctwcon%5Es1_&ref_url=https%3A%2F%2Fgnews.org%2F1062692

    lab-produced virus

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    IveyTech

    Member
    April 14, 2021 at 3:03 pm

    Rather than speculate as an untrained person, I have provided some excerpts.

    “The most pronounced difference between SARS-S and SARS-2-S is an additional furin cleavage site (site 1, Figure 2A) resulting from an insertion of 12 nt at the boundary between S1 and S2 [8,11,29]. This additional furin cleavage site is shared among all sequenced SARS-CoV-2 genomes, but absent in all their closest known relatives such as bat RaTG13 and those isolated from pangolin [29]. The seemingly sudden appearance of this additional polybasic furin cleavage site 1 has been a lasting source of conspiracy theory that SARS-CoV-2 is man-made, which is discussed later.”

    “…The furin cleavage site was predicted in February 2020 [8] and, in May 2020, its functional importance was confirmed, i.e., that the cleavage was essential for efficient viral entry into human lung cells[…]”

    “…In addition to site 1 and site 2 (Figure 2A) that cleave SARS-2-S into the S1 and S2 domains, a third cleavage site also exists for cleaving S2 into FP and S2′ domains (Figure 2B,D). This site, often referred to as the S2′ site, is likely cleaved by TMPRSS2 [41,42,43,44], consistent with the finding that TMPRSS2 is needed for SARS-CoV-2 infection[…]”

    “As previously mentioned, the additional polybasic furin cleavage site 1 (Figure 2A) has been a lasting source of conspiracy theory that SARS-CoV-2 is man-made. Advocates of the conspiracy theory assume that scientists have ignored or refused to address their legit concerns[…]”

    “…First, the furin cleavage site has not been observed in any close relatives of SARS-CoV-2 in nature. A somewhat similar furin cleavage site was present at a roughly homologous site in S protein of the murine hepatitis virus [45] and in a few alphacoronaviruses [2,8,29]. However, it is not clear how SARS-CoV-2 could gain it from these remote relatives. While recombination might be a possibility, there is hardly any sequence homology between SARS-2-S and its homologues in the murine hepatitis virus or alphacoronaviruses at sequences flanking the cleavage site, therefore, a recombination origin of the cleavage site is tenuous at present. An insertion at the same site was found in a bat-derived coronavirus [92], but the inserted sequence was different and could not function as a furin cleavage site. A novel bat-derived coronavirus (RmYN02) was reported to have an insertion bearing a weak semblance to the polybasic furin cleavage site in Figure 2A [92], suggesting the possibility of a natural origin of the polybasic furin cleavage site. However, the sequence homology between RmYN02 and SARS-2-S is low, and it is not clear if the insertion in RmYN02 is real or an artefact of alignment. Therefore, if one cannot offer a plausible hypothesis of natural origin of the polybasic site, it is easy to fall back on the hypothesis of artificial origin. This reminds us of the period of time before Darwin, i.e., when the origin of species cannot be fully explained, it is easy to fall back to the theory of a creator.

    The second reason for the conspiracy theory is associated with the feasibility of creating such a polybasic site and a need to create such a site for testing certain biological hypotheses. Some background information arising from SARS-S is needed to understand this reason. The roughly homologous RNA segment in SARS-S is a weak cleavage site, likely cleaved by transmembrane serine protease TMPRSS2 [93]. R667 in SARS-S (immediately upstream of the site 1 cleavage in Figure 2A) is required for cleavage by TMPRSS2 [93]. The site can also be cleaved by trypsin, and processing of SARS-S by trypsin enhances viral infectivity [34,45,94]. Because trypsin and trypsin-like proteases are strongly tissue restricted (Figure 2C), the site is typically not cleaved in SARS-S [24]. It is natural for one to hypothesize that adding a furin cleavage site would allow the site to be efficiently cleaved in nearly all tissues, potentially enhancing SARS-CoV infection and broadening its cell tropism. Indeed, introducing a furin cleavage site at the S1 and S2 boundary of SARS-S has increased cell-cell fusion (syncytium formation) and viral infectivity [34]. This result suggests that the additional polybasic furin cleavage site may have contributed significantly to the efficiency of SARS-CoV-2 in infecting human. Host cells, in response to viral infection, may reduce furin activities [8].

    In short, given the seemingly sudden appearance of the additional furin cleavage site that cannot be readily explained by a hypothesis of natural origin, and the fact that virologists have already experimented with adding a furin cleavage site at this specific location and learned the consequence of enhanced viral infectivity and cell-cell fusion, the claim that the polybasic furin cleavage site in SARS-2-S has been experimentally inserted is not too far-fetched. However, the global collaboration among scientists, in general, and virologists, in particular, has created scientific communities that are far more closely knit than before. While it is possible to create a viral pathogen, it is extremely unlikely for a laboratory to create SARS-CoV-2 without being noticed.

    The third reason is that the 12 nt insertion encoding the polybasic furin cleavage site carries two CpG dinucleotides. Such CpG dinucleotides are very rare in SARS-CoV-2 [95], and particularly rare in SARS-2-S. Why would such CpG rarity contribute to the conspiracy theory? Mammalian zinc finger antiviral protein (ZAP, gene name ZC3HAC1) targets CpG dinucleotides in viral RNA to mediate RNA degradation and inhibit viral replication [96]. The ZAP-mediated RNA degradation is cumulative [96], as shown by the following experiment. When CpG dinucleotides were experimentally added to individual viral segment 1 or 2, the inhibitory effect of ZAP was weak. However, when the same CpG dinucleotides were added to both segments 1 and 2, the ZAP inhibition effect was strong [96]. This implies that only mRNA sequences of sufficient length would be targeted by ZAP (i.e., S, 1ab, and 1a mRNAs in SARS-CoV and SARS-CoV-2). SARS-CoV-2 and its closest relatives from bat (RaTG13) and pangolin exhibit the strongest genomic CpG deficiency among all betacoronaviruses [95], presumably to evade ZAP-mediated host defense. The S gene is particularly CpG-deficient as measured by two indices, I<sub>CpG</sub> [95,97] and ln (N<sub>CG</sub>/N<sub>GC</sub>) (Table 1), where N<sub>CG</sub> and N<sub>GC</sub> are the numbers of CpG and GpC dinucleotides in the S gene. I<sub>CpG</sub> < 1, or ln (N<sub>CG</sub>/N<sub>GC</sub>) < 0, means CpG deficiency.

    Table 1

    Genomic CpG deficiency in the coding sequence encoding the spike proteins, measured by two indices: I<sub>CpG</sub> = (P<sub>C</sub>*P<sub>G</sub>/P<sub>CG</sub>) and ln (N<sub>CG</sub>/N<sub>GC</sub>). The expectation of no CpG deficiency is 1 for I<sub>CpG</sub> and 0 for ln (N<sub>CG</sub>/N<sub>GC</sub>).

    Because of this ZAP-mediated selection against CpG, SARS-CoV-2 and its close relatives encode most of arginine residues by the two AGR codons, instead of the four CGN codons. The S gene encodes 42 arginine residues, with only 12 (28.57%) encoded by the four CGN codons in contrast to 30 encoded by the two AGR codons. The two arginine residues in the polybasic furin cleavage site are encoded by the rare CGN codons, which seems unnatural in this context. However, the probability of randomly picking up two arginine codons that happen to be both CGN codons is not extremely low (i.e. =0.2857<sup>2</sup> = 0.0816).

    One way to dispel the conspiracy theory is to find a set of viral lineages in wildlife that would allow reconstruction of a plausible evolutionary path leading to the origin of the polybasic furin cleavage site[…]

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7829931/#!po=43.9597

    (See the source at the discussion about “Is Moderna vaccine safe in the long term” as it pertains to vaccines)

    – – – – – –

    Also there is a “war” of research virologists/immunologists amongst themselves about what the RaTG13 written genome sequence really is (no actual sample exists?). The furin cleavage site is a point of disagreement whether it is a “smoking gun” pointing towards artificial mutation, also known as “gain-of-function” of a virus. Why would a virus have the evolutionary intelligence to jump species being that it has no classic “desire” to survive nor produce offspring for its posterity? Move a few letters, add a few letters of DNA…but what designed and foresaw the virus’ survival? “P-o-s-t-e-r-i-t-y” becomes “preposterous” by shifting your point of view and also by moving/changing/adding/subtracting the building blocks (letters).

    Q. So how about a lab scientist deliberately moving DNA building blocks around…if you can see the analogy.

    The link to https://mobile.twitter.com/DrLiMengYAN1?ref_src=twsrc%5Etfw%7Ctwcamp%5Etweetembed%7Ctwterm%5E1379813194156408837%7Ctwgr%5E%7Ctwcon%5Es1_&ref_url=https%3A%2F%2Fgnews.org%2F1062692

    lab-produced virus

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    IveyTech

    Member
    May 3, 2021 at 5:02 pm
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    IveyTech

    Member
    May 3, 2021 at 5:24 pm

    That the WHO team is keeping the frozen food theory alive is sure to please some in the Chinese government. Some officials and state media in China have promoted a so-called “multiple-origin” scenario, according to CNN, where the pandemic started with outbreaks in different parts of the world. The report however, is sure to disappoint the scientists, researchers, and officials who suspect a lab leak could have started the pandemic.

    And officials in Washington and elsewhere quickly cast doubt on the WHO team’s conclusions. Fourteen countries, including the United States, Japan, and the United Kingdom issued a joint statement saying they were concerned that “the international expert study on the source of the SARS-CoV-2 virus was significantly delayed and lacked access to complete, original data and samples.”

    The Twitter account that is miraculously not suspended:

    https://mobile.twitter.com/DrLiMengYAN1

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