#1 - Wuhan (Novel) Corona Virus - looming pandemy of deadly pneumonia?

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I understand the criticism of the 2020 Pradhan paper, but it finally clicked (in my simian brain) how unusual (unfortuitous) that the four S-protein segment insertions really are. Maybe I got this wrong:

1) They're all in different places on the S-protein, rather than in a continuous segment.

2) The chances are pretty remote that ANY random set of two or three, much less four small inserts somewhere along the S-protein would leave it functional AT ALL. It would be expected that such a set of inserts would deactivate it or otherwise alter its function for the worse.

3) These new four inserts incredulously leave the S-protein's existing function perfectly intact, specifically it's critical ACE2 binding affinity (same as SARS). What are the chances that a random 4-segment insert doesn't change the binding surface, but only adds previously unseen functionality to a coronavirus S-protein?

4) Those new segments 1) ADD binding affinity for human white blood cells (T-cells) at the CD4 site, ADD the capability to invade and corrupt T-cell functionality to make it produce yet more coronavirus, and CREATES a high affinity binding site for a chemokine co-receptor like CXCR4 and/or CCR5.

The paper's authors describe the four inserts relation to HIV, but (from what I read) its nearly impossible for those four particular segments to have been produced naturally by some mutation with HIV or anything else and miraculously produce such an enhanced S-protein.

To your point, Bruce:

"The unique biological properties that HIV sequences could theoretically impart to another virus are completely missing from 2019-nCoV [Like infection and mortality?], and 2019-nCoV has no unique clinical properties that are outside what is known to be possible for a coronavirus."

Those sequences' theoretically imparted unique biological properties ARE there, according to The Lancet in this article:

Are Pradhan et. al.’s findings right or wrong? If correct, the virus should be able to invade human CD4 T cells and result in corresponding clinical features. A paper published in The Lancet on Jan. 24, 2020 by Professor Chaolin Huang from Jin Yin-tan Hospital, Wuhan, China, et. al., reviewing “Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China” supports Pradhan et. al’s conclusions.

...

Although low white blood cell counts are common in viral infections, it is surprising that 63 percent of all infected patients and 85 percent of those admitted to the ICU had lymphopenia with lymphocyte counts <1·0 × 109/L. In a study on SARS published March 2004 by C.M. Chu et. al. in the journal Thorax, the mean lymphocyte count was often reported as normal.

On Jan. 22, 2020, two clinical guidelines for the diagnosis and treatment of Wuhan 2019-nCoV were posted on China websites. One is “Quick Guide for the Diagnosis and Treatment of New Coronavirus Pneumonia” authored by the expert group of Tongji Hospital, and the other is “Instructions for Handling 2019 New Coronavirus” from the Wuhan Union Hospital of Tongji Medical College of Huazhong University of Science and Technology. The first guideline clearly points out a “progressive lymphocyte reduction” while the second guideline highlights “the importance of monitoring the absolute value of lymphocytes.” (emphasis added)

Therefore, the observed lymphocyte reduction must be of clinical significance in a certain proportion of patients. CD4 positive T lymphocytes constitute a major fraction of all lymphocytes. Although not a routine test for patients with coronavirus infection, perhaps monitoring CD4 cell counts would be helpful in 2019-nCoV patients.

nCoV attacks lymphocytes reducing counts UNLIKE SARS or other coronaviruses. How about the CXCR4 and/or CCR5 and resulting cytokine storm and respiratory distress?

Another clinical feature of patients infected with 2019-nCoV is the high levels of serum cytokines and chemokines, which is defined as a cytokine storm (Huang et al 2020 Lancet). This is consistent with the observation from Pradhan et al. that the 2019-nCoV S-protein inducing structural rearrangements in GP120, creating a high affinity binding site for a chemokine co-receptor such as CXCR4 and/or CCR5. It is well known that activating T cell surface receptors can cause a cytokine storm. Cytokine storms have potential to create significant damage to organs and bodily tissues. If a cytokine storm occurs in the lungs, for example, immune cells such as macrophages and fluid may trigger tissue damage that results in acute respiratory distress and possible death.

Sounds like the result of those unique biological properties since doctors are distinguishing nCoV presentation with what they have seen in SARS.

Improbable for this mutation to have occurred naturally. And if I was and evil bioweapons engineer/scientist trying to 'enhance' SARS, I might just look for 1) someplace insert a few segments in the spike protein without screwing it up, and 2) something particularly nasty to insert in those segments, like gp120 and gag from HIV.

And it occurs to me that you all have probably already concluded as much in earlier posts - it all just flew over my head. Sorry!

@b

Read PaveWayIV's technical explanation, the Indians were right, they retracted the paper to have it updated and publish it when it is ready.

The debunkers of the Indian research paper BLAST-ed each insertion "one by one" to find resemblance with a variety of organisms not just HIV but what are the chances of a combination of 4 insertions to resemble HIV?

According to the reports, there would be three kinds of species that would have to be involved. An African cobra, a rare South Pacific bat, and some kind of sea-creature.

Plus 4 HIV inserts are not a natural occurrence.
https://www.moonofalabama.org/2020/02/coronaupdate.html?cid=6a00d8341c640e53ef0240a4bac7ea200c#comment-6a00d8341c640e53ef0240a4bac7ea200c

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