On the Origins of Covid

It’s entirely reasonable to ask you to actually cite what you’re referring to. You tried once already, it ended up not being true.

This is being done for a reason btw. I want you to specifically support your assertion and pin you down on a falsifiable position. I don’t care about the VF article or the article written by some piece of shit racist, they aren’t serious scientific pieces and aren’t worth paying attention to.

However, if you’re going to use those articles to support your argument, I want you to pick out what you think is important. Otherwise I’m left guessing at what you mean or are referring to. That’s fine when it’s a page or two, but when it it comes out to ~40-45 pages in print preview that’s not a fair ask.

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Guy whose contributions of outside source materials and reputable links consists entirely of a single twitter thread is demanding a fully cited and auditable academic trail for any and all comments.

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That, of course, is a complete lie. I’m asking for the specific part of the 40+ page article that he thinks supports his position after he chose one that didn’t support his assertion.

How this is unreasonable to anyone here?

lmfao.

“They were funding GoF research!”

“Where does it say that?”

“I’m not playing these games with you!”

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Francis Collins is also in on the conspiracy, it seems.

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https://www.nature.com/articles/nm.3985

2015 paper where Shi is a co-author.

“ Using the SARS-CoV reverse genetics system2, we generated and characterized a chimeric virus expressing the spike of bat coronavirus SHC014 in a mouse-adapted SARS-CoV backbone. The results indicate that group 2b viruses encoding the SHC014 spike in a wild-type backbone can efficiently use multiple orthologs of the SARS receptor human angiotensin converting enzyme II (ACE2), replicate efficiently in primary human airway cells and achieve in vitro titers equivalent to epidemic strains of SARS-CoV. Additionally, in vivo experiments demonstrate replication of the chimeric virus in mouse lung with notable pathogenesis. Evaluation of available SARS-based immune-therapeutic and prophylactic modalities revealed poor efficacy; both monoclonal antibody and vaccine approaches failed to neutralize and protect from infection with CoVs using the novel spike protein. On the basis of these findings, we synthetically re-derived an infectious full-length SHC014 recombinant virus and demonstrate robust viral replication both in vitro and in vivo . Our work suggests a potential risk of SARS-CoV re-emergence from viruses currently circulating in bat populations.”

Describing creating chimeric viruses in a lab with a spike protein that makes it more infectious to humans.

In addition to offering preparation against future emerging viruses, this approach must be considered in the context of the US government–mandated pause on gain-of-function (GOF) studies22. On the basis of previous models of emergence (Fig. 4a,b), the creation of chimeric viruses such as SHC014-MA15 was not expected to increase pathogenicity. Although SHC014-MA15 is attenuated relative to its parental mouse-adapted SARS-CoV, similar studies examining the pathogenicity of CoVs with the wild-type Urbani spike within the MA15 backbone showed no weight loss in mice and reduced viral replication23. Thus, relative to the Urbani spike–MA15 CoV, SHC014-MA15 shows a gain in pathogenesis (Fig. 1). On the basis of these findings, scientific review panels may deem similar studies building chimeric viruses based on circulating strains too risky to pursue, as increased pathogenicity in mammalian models cannot be excluded.

Acknowledging that what they did was GoF research and may conflict with the then-existing US ban on that type of research.

Research in this manuscript was supported by grants from the National Institute of Allergy & Infectious Disease and the National Institute of Aging of the US National Institutes of Health (NIH) under awards U19AI109761 (R.S.B.), U19AI107810 (R.S.B.), AI085524 (W.A.M.), F32AI102561 (V.D.M.) and K99AG049092 (V.D.M.),

But this research was in fact funded by NIH

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So yes. It appears she is in on it too. I don’t know what to tell you, it’s a hard day when you learn for the first time that the government sometimes lies to you.

So you’re citing work done in the USA to call Fauci a liar for saying the NIH didn’t support gain of function work in Wuhan and the creation of a virus modifying with a mouse virus to say the NIH is lying when the “NIH nor NIAID have ever approved any grant that would have supported “gain-of-function” research on coronaviruses that would have increased their transmissibility or lethality for humans.”

Once again, you not understanding what you’re reading has led you to an erroneous position. If you have any other questions, let me know.

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The work in the paper was done both in the US and at WIV.

And the mice being used had humanized lung tissue. The virus wasn’t “modified with a mouse virus” it was bat coronavirus modified with a spike protein from a different bat coronavirus that was known to be infectious to humans in the same way the sars-cov2 spike protein is. Like, you’ve been fucking gaslighting me about the things I’ve posted on this topic for weeks.

Edit: I might be wrong on the humanized mice for this experiment. Looks like regular mice and then just human tissue samples.

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The lab work done in that paper that you’re concerned about was in North Carolina. You’re simply wrong about that. Feel free to show otherwise. You, again, don’t know what you’re talking about.

Using the SARS-CoV reverse genetics system2, we generated and characterized a chimeric virus expressing the spike of bat coronavirus SHC014 in a mouse-adapted SARS-CoV backbone.

I suppose my post was sloppily worded, but that’s not a human SARS virus either.

‘Humanized’ lung tissue is also, you know, not human lung tissue.

I think it’s fair to question if that type of research is a good idea, and frankly, it’s beyond what I’m willing to really definitively weigh in on. The only way you could use that paper to support Rand Paul’s statement or call the NIH a liar is through ignorance however.

I was wrong about what this says. Still mad at ikes tho

Viruses, cells, in vitro infection and plaque assays.

Wild-type SARS-CoV (Urbani), mouse-adapted SARS-CoV (MA15) and chimeric SARS-like CoVs were cultured on Vero E6 cells (obtained from United States Army Medical Research Institute of Infectious Diseases), grown in Dulbecco’s modified Eagle’s medium (DMEM) (Gibco, CA) and 5% fetal clone serum (FCS) (Hyclone, South Logan, UT) along with antibiotic/antimycotic (Gibco, Carlsbad, CA). DBT cells (Baric laboratory, source unknown) expressing ACE2 orthologs have been previously described for both human and civet; bat Ace2 sequence was based on that from Rhinolophus leschenaulti , and DBT cells expressing bat Ace2 were established as described previously8. Pseudotyping experiments were similar to those using an HIV-based pseudovirus, prepared as previously described10, and examined on HeLa cells (Wuhan Institute of Virology) that expressed ACE2 orthologs.

I suppose I could be wrong, but that sure appears to be the source of the HeLa cells, given that literally everything else in that part of the paper is a source. It’d be weird as hell to do all the lab work in NC and fly across the world with a virus in a level 3 facility.

I read this one, carefully. You still don’t understand it.

They don’t say that at all, seriously wtf are you smoking.

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Yeah idk on reread you’re probably right. I read the baric lab, source unknown part and thought it was listing labs for each but it seems like sources.

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30 March 2020 Editors’ note, March 2020: We are aware that this article is being used as the basis for unverified theories that the novel coronavirus causing COVID-19 was engineered. There is no evidence that this is true; scientists believe that an animal is the most likely source of the coronavirus

Chef’s kiss.

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As near as I can tell this is a study done in North Carolina showing a bat virus can very easily infect mice with receptors made to mimic human receptors. There’s no “gain of function” to make it more infectious and no suggestion they were breaking any rules. If anything, this work adds a whole lot of credence to the theory that these viruses can jump to humans without Chinese biolabs making secret weapons.

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Serious question.

In the rare instance that this was a lab leak couldn’t gain of function research still be really important and we should continue to do it?

I don’t know enough about it but it seems gain of function is kind of being thrown around as a buzz word.

The risks from gain-of-function mutations, at least on whole viruses, are pretty large compared with the benefits, at least in the short term. Let’s say you find a bat virus, induce a mutation, and then find that the mutation makes it highly infectious to humans. What’s the plan, then? Vaccinate everyone against that? Well, that’s pretty damn expensive, and unless you’re going to share with literally everyone on the planet, and not just, say, your own country, you’re going to get accusations of designing a bioweapon. Are you going to do that for every functional mutation you find? That’s going to add up quickly, and you can pump out new mutations faster than we can verify the safety and efficacy of a new vaccine and then pump out 7 billion doses. Essentially anything you’d design, whether vaccine or small molecule drug, would take considerable expense to produce and would be largely worthless unless it actually did turn into a pandemic, and if you actually start a pandemic with a new mutation, then the prior vaccines and drugs may be ineffective and again a waste of effort.

There’s potentially some good work that can be done on gain-of-function mutants of isolated proteins from the virus, but you don’t need to have viruses that can infect cells in order to do that. You can have bacteria or yeast produce those proteins en masse for you from templates that contain only the code for just those proteins on plasmids. For example, you could do random mutagenesis on just the spike protein and find sequences that don’t bind human antibodies generated by the immune response to one or more of the vaccines and crosscheck those for the continued ability to bind ACE2. That could potentially alert you to some sequences that would be cause for extra alarm should they pop up in viral surveillance sequencing, and there’s no risk of starting a pandemic with it (outside of someone literally and maliciously manipulating whole viruses according to your data to (re-)start a pandemic, I suppose).

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Thanks for taking the time to write this. It gives me a better understanding.

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Nature’s take:

https://www.nature.com/articles/d41586-021-01529-3

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