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yall covid-19 response isn't about this administration or the current political mood. it's about a consistent racist, classist disregard for the health of *everyone* on the part of the poeople holding money and power.

back when SARS-CoV-1 was a thing 20 years ago, people got inundated with money to work on it just like people are for COVID-19 (SARS-CoV-2). and then the SARS-1 epidemics burnt out, because it was way more fatal which is a *shitty* thing for a virus to be. and people in power forgot about it, because it didn't matter that a few people died or whatever, while scientists (sometimes, literally) *screamed* in their faces that there was a high probability of another zoonotic spillover ~soon that would be way worse. so anyone working on SARS-type coronaviruses got back-shelf funding.

and guess what happened? SARS-CoV-2. they've ignored nature's inevitable path of optimization, and said, oh, we'ven't had a big epidemic in the US for ~100y! just. disgusting. fuckin. hubris.

also yeah if yall didn't know this? the thing people called SARS? COVID-19 is basically that but 2.0. SARS is now called SARS-CoV-1, whereas COVID-19's virus is called SARS-CoV-2. we could've had a vaccine ready if funding and time had been poured in over the last twenty years, and we had every reason to suspect this would happen.

the only reason we called it COVID-19 and not SARS-2 is that politicians wanted to make it sound nicer. not like something fucking terrifying like SARS. which. you know what? we should've picked the terrifying name to try to make people care.

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@er1n covid-19 was suuuch a terrible name, especially given the alternative readily available!

@er1n @velexiraptor My understanding from a light googling is that SARS and COVID-19 are not related except being produced by viruses in the same general family, and research in one would seem unlikely to yield results in the other. SARS attacks the lungs specifically; the running hypothesis for COVID-19 is that it is an blood vessel infection.

@er1n @velexiraptor there are enough real reasons to be angry at the people who govern us and the ways they oppress us to add to that hurt reasons that do not correspond to real needs.

@millenomi @velexiraptor it has rly high sequence conservation and the receptor binding domain/spike glycoprotein of SARS-CoV-1/2 align very, very well. also, research in SARS-CoV-1 has produced results in SARS-CoV-2, cf the proline substitution in the S protein locking it into pre-fusion state and increasing its antigenicity by ~10x (this was first done in -1, now deployed in -2 work particularly in mRNA vaccines)

@er1n @velexiraptor I need to better inform myself then. Do you have links?

@millenomi @velexiraptor i used to have access to a Barney Graham talk from a conf earlier this spring (WVCW) which had some good history, but i don't now unfortunately

here's a paper i haven't used before that talks about sequence conservation (noting that the transmembrane domain is conserved): ncbi.nlm.nih.gov/pmc/articles/

also note that one of the big issues with developing coronavirus vaccines is that they're just. really hard to work with compared to flu, and even in flu very few companies do the genetic rescue work needed to make this stuff precisely. traditionally you just kinda, inactivate the virus chemically and then put the mangled bits in someone and hope it elicits immunity, but that doesn't seem to work at *all* with respiratory coronaviruses in general

@millenomi @velexiraptor the one big thing, regardless, that more work into sars-cov-1 would've done is an effective antiviral. coronaviruses have a proofreader so that even if you use nucleoside analogs to gum up the transcriptases and make faulty copies, they get corrected. this is part of why remdesivir is trash

@millenomi @velexiraptor *some coronaviruses; sars-cov-1 definitely did. i don't actually know if it's *all*, since i'm computers and maths girl who got hired to do programmeing work on a vaccine project

@millenomi @velexiraptor also yeah SARS-CoV-1 and SARS-CoV-2 are part of the same lineage in the sense that they're part of the small subset of respiratory coronaviruses that bind with high specificity to human ACE2

@millenomi @velexiraptor also, from one of the Big papers on the COVID-19 outbreak:

> Notably, we confirmed that 2019-nCoV uses the same cell entry receptor—angiotensin converting enzyme II (ACE2)—as SARS-CoV.
nature.com/articles/s41586-020

@millenomi @velexiraptor also i should probably stop flooding you but i uh. work with several people i highly trust in the biological sciences who are pretty fucking sure we could've prevented this if anyone cared about respiratory coronaviruses for the last 20 years; it's easier to get money for the flu because you can make money off of selling shit yearly! that's not the case for this stuff when there's no profit incentive without an epidemic

@millenomi @velexiraptor i mean, we could've prevented this entire mess by actually having working health systems and not forcing people to work and participate in a society that grinds them up and kills them, especially if they're marginalised

@millenomi @velexiraptor also part of the suspicion with blood vessel stuff is, yeah, that it might be attacking that, but also i've heard that there's no indication of virema in most patients according to PCR, so my suspicion is that blood vessel problems could also be caused by self-immunization or some kind of cytokine storm

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