Wuhan Virus Update

The link in that article purporting that "Biologists Botao Xiao and Lei Xiao published a pre-print entitled “The possible origins of 2019-nCoV coronavirus.” claiming that it was engineered in the lab was later retracted by those authors for lack of evidence. It isn't credible at all.

The Russians having a vaccine supposedly created in a "secret bio-weapons lab" to COVID-19 is zero proof that the virus itself isn't anything other than naturally occurring. A vaccine would be made the same way to a virus whether it was natural or not.

The 3rd/4th link in that article, where China blamed the U.S. military for releasing SARS-CoV-2 in China is the Chinese Communist Party being assholes trying to blame us for their problems. They can f*** off.

That last link is about an assertion that a Taiwanese researcher made that the addition of 4 amino acids was unusual and lent credence to it being man-made was debunked by other researchers, and that same Taiwanese researcher later denied making the claim that it was man-made. Note too, that he made that assertion in February and the articles I cited came out afterwards demonstrating deeper and more reliable genetic analyses published in more credible journals.

Taiwanese professor says Wuhan coronavirus likely man-made

The professor said that viruses normally only have small mutations in the form of singular changes in natural conditions. He asserted that in nature, it is "unlikely to have four amino acids added at once."

Fang concluded, "Therefore, from an academic point of view, it is indeed possible that the amino acids were added to COVID-19 in the lab by humans." He said that it is also still possible that this occurred in nature but that "the chances are very slim."

However, renowned Taiwanese-American professor Ching Lin on Feb. 1 refuted a similar theory being circulated that it was "bioweapon" created by the U.S., saying the addition of the aforementioned four amino acids is not as "critical" as some in the Chinese media had claimed.

Lin also cast doubt on the credibility of the paper (Uncanny similarity of unique inserts in the 2019-nCoV spike protein to HIV-1 gp120 and Gag) being cited in the conspiracy theories. He first suggested that the platform bioRxiv, on which the paper was published, is untrustworthy as most of the literature it posts does not undergo peer review.

After being contacted by Taiwan News for comment, Fang denied making the previously cited statements and said that he "does not support the highly popular man-made theory on the origin of this virus."

1. This is about MERS, which arrived back in 2012. Read the comments in that article, it's trash.

nate303 wrote: sphcm.med.unsw.edu.au/news/could-mers-co...planations-paradoxes

2.

nate303 wrote: thediplomat.com/2020/04/did-xi-jinping-d...ly-sicken-the-world/

From that article:

None of this can prove whether or when Xi made a deliberate decision to withhold information in order to imperil others. ...This may constitute biological warfare. But even if it doesn’t Xi should be brought to account

Opinion article. Not evidence.


3.

nate303 wrote: onlinelibrary.wiley.com/doi/10.1111/1469-8676.12799

Ken Alibek - Former Soviet Bio Weapons Chief Scientist

From that article:

We don’t know if Wuhan Institute conducts the secret research it was accused of, but we know that 30 years ago the Soviet centre for virology and microbiology, Vector, did.

This is Russia, not China, and again, there's no evidence cited that China engineered this virus.


4.

nate303 wrote: www.foxbusiness.com/healthcare/pandemic-...irus-sars-ken-alibek

No where in this story is the assertion made that China deliberately created this virus. Did they hide the initial outbreak? Absolutely. But we still don't know why, where it's natural host reservoir is, and what was being studied in the Wuhan lab. All genetic analysis points to it being a natural virus that evolved in multiple animal hosts before gaining the ability to infect humans, as all other natural viruses do.

For some good news about COVID-19:
Steroids reduce deaths of critically ill COVID-19 patients, WHO confirms
The finding strengthens evidence that clinicians should give severely sick people the drugs
By Tina Hesman Saey, Science News | September 2, 2020

In June, a large study in the United Kingdom suggested that the steroid dexamethasone could help reduce the risk of death for critically ill COVID-19 patients. Now, more evidence suggests that steroids are an effective weapon against the coronavirus.

Researchers from the World Health Organization combined data from seven randomized clinical trials for severely or critically ill COVID-19 patients treated with steroids versus standard care or a placebo up to June 9. The trials used the steroids hydrocortisone, dexamethasone or methylprednisolone.

And this was fascinating. My lab director and former boss shared this one:
A Supercomputer Analyzed Covid-19 — and an Interesting New Theory Has Emerged
A closer look at the Bradykinin hypothesis
Thomas Smith, Medium

Earlier this summer, the Summit supercomputer at Oak Ridge National Lab in Tennessee set about crunching data on more than 40,000 genes from 17,000 genetic samples in an effort to better understand Covid-19. Summit is the second-fastest computer in the world, but the process — which involved analyzing 2.5 billion genetic combinations — still took more than a week.

When Summit was done, researchers analyzed the results. It was, in the words of Dr. Daniel Jacobson, lead researcher and chief scientist for computational systems biology at Oak Ridge, a “eureka moment.” The computer had revealed a new theory about how Covid-19 impacts the body: the bradykinin hypothesis. The hypothesis provides a model that explains many aspects of Covid-19, including some of its most bizarre symptoms. It also suggests 10-plus potential treatments, many of which are already FDA approved. Jacobson’s group published their results in a paper in the journal eLife in early July.

According to Jacobson’s group, the data Summit analyzed shows that Covid-19 isn’t content to simply infect cells that already express lots of ACE2 receptors. Instead, it actively hijacks the body’s own systems, tricking it into upregulating ACE2 receptors in places where they’re usually expressed at low or medium levels, including the lungs.

In this sense, Covid-19 is like a burglar who slips in your unlocked second-floor window and starts to ransack your house. Once inside, though, they don’t just take your stuff — they also throw open all your doors and windows so their accomplices can rush in and help pillage more efficiently.

The paper:
A mechanistic model and therapeutic interventions for COVID-19 involving a RAS-mediated bradykinin storm
Michael R Garvin, Christiane Alvarez, J Izaak Miller, Erica T Prates, Angelica M Walker, B Kirtley Amos, Alan E Mast, Amy Justice, Bruce Aronow, Daniel Jacobson
Jul 7, 2020
Cite as: eLife 2020;9:e59177 doi: 10.7554/eLife.59177

Neither the disease mechanism nor treatments for COVID-19 are currently known. Here, we present a novel molecular mechanism for COVID-19 that provides therapeutic intervention points that can be addressed with existing FDA-approved pharmaceuticals. The entry point for the virus is ACE2, which is a component of the counteracting hypotensive axis of RAS. Bradykinin is a potent part of the vasopressor system that induces hypotension and vasodilation and is degraded by ACE and enhanced by the angiotensin1-9 produced by ACE2. Here, we perform a new analysis on gene expression data from cells in bronchoalveolar lavage fluid (BALF) from COVID-19 patients that were used to sequence the virus. Comparison with BALF from controls identifies a critical imbalance in RAS represented by decreased expression of ACE in combination with increases in ACE2, renin, angiotensin, key RAS receptors, kinogen and many kallikrein enzymes that activate it, and both bradykinin receptors. This very atypical pattern of the RAS is predicted to elevate bradykinin levels in multiple tissues and systems that will likely cause increases in vascular dilation, vascular permeability and hypotension. These bradykinin-driven outcomes explain many of the symptoms being observed in COVID-19.