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Those fun loving chicoms

WestlinnDuckWestlinnDuck Member Posts: 15,703 Standard Supporter
Maybe Slo Jo can explain again how we are not in a competition with the chicoms. Once you buy a Biden they stay bought. We will see how this plays out. Easier to blame bat stew. Chicoms have been stealing viruses. Wuhan does have a major bio facility. Dr. Peng was playing around with bat corona viruses.

https://www.zerohedge.com/geopolitical/coronavirus-contains-hiv-insertions-stoking-fears-over-artificially-created-bioweapon

Coronavirus Contains "HIV Insertions", Stoking Fears Over Artificially Created Bioweapon
Over the past few days, the mainstream press has vigorously pushed back against a theory about the origins of the coronavirus that has now infected as many as 70,000+ people in Wuhan alone (depending on whom you believe). The theory is that China obtained the coronavirus via a Canadian research program, and started molding it into a bioweapon at the Institute of Virology in Wuhan. Politifact pointed the finger at Zero Hedge, in particular, though the story was widely shared across independent-leaning media.
The theory is that the virus, which was developed by infectious disease experts to function as a bio-weapon, originated in the Wuhan-based lab of Dr. Peng Zhou, China's preeminent researcher of bat immune systems, specifically in how their immune systems adapt to the presence of viruses like coronavirus and other destructive viruses. Somehow, the virus escaped from the lab, and the Hunan fish market where the virus supposedly originated is merely a ruse.

Now, a respected epidemiologist who recently caught flack for claiming in a twitter threat that the virus appeared to be much more contagious than initially believed is pointing out irregularities in the virus's genome that suggests it might have been genetically engineered for the purposes of a weapon, and not just any weapon but the deadliest one of all.
In "Uncanny similarity of unique inserts in the 2019-nCoV spike protein to HIV-1 gp120 and Gag", Indian researchers are baffled by segments of the virus's RNA that have no relation to other coronaviruses like SARS, and instead appear to be closer to HIV. The virus even responds to treatment by HIV medications.
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Why do the authors think the virus may be man-made? Because when looking at the above insertions which are not present in any of the closest coronavirus families, "it is quite unlikely for a virus to have acquired such unique insertions naturally in a short duration of time." Instead, they can be found in cell identification and membrane binding proteins located in the HIV genome.

Since the S protein of 2019-nCoV shares closest ancestry with SARS GZ02, the sequence coding for spike proteins of these two viruses were compared using MultiAlin software. We found four new insertions in the protein of 2019-nCoV- “GTNGTKR” (IS1), “HKNNKS” (IS2), “GDSSSG” (IS3) and “QTNSPRRA” (IS4) (Figure 2). To our surprise, these sequence insertions were not only absent in S protein of SARS but were also not observed in any other member of the Coronaviridae family (Supplementary figure). This is startling as it is quite unlikely for a virus to have acquired such unique insertions naturally in a short duration of time.

The insertions were observed to be present in all the genomic sequences of 2019-nCoV virus available from the recent clinical isolates. To know the source of these insertions in 2019-nCoV a local alignment was done with BLASTp using these insertions as query with all virus genome. Unexpectedly, all the insertions got aligned with Human immunodeficiency Virus-1 (HIV-1). Further analysis revealed that aligned sequences of HIV-1 with 2019-nCoV were derived from surface glycoprotein gp120 (amino acid sequence positions: 404-409, 462-467, 136-150) and from Gag protein (366-384 amino acid) (Table 1). Gag protein of HIV is involved in host membrane binding, packaging of the virus and for the formation of virus-like particles. Gp120 plays crucial role in recognizing the host cell by binding to the primary receptor CD4.This binding induces structural rearrangements in GP120, creating a high affinity binding site for a chemokine co-receptor like CXCR4 and/or CCR5.
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