We've discussed this at least twice, if not more. What works in a petri dish doesn't necessarily work in a real person (especially when tested on a different virus). And the evidence looks very good that this is one of the many, many things someone found out didn't translate from in vitro to in vivo. It's not just that, but it's a fringe hypothesis even in terms of the in vitro data.Zn(2+) inhibits coronavirus and arterivirus RNA polymerase activity in vitro and zinc ionophores block the replication of these viruses in cell culture - PubMed
Increasing the intracellular Zn(2+) concentration with zinc-ionophores like pyrithione (PT) can efficiently impair the replication of a variety of RNA viruses, including poliovirus and influenza virus. For some viruses this effect has been attributed to interference with viral polyprotein...pubmed.ncbi.nlm.nih.gov
If it works against SARS-COV-1, it most probably works for SARS-COV-2.
It's exactly the logic of steroids. You don't want to give someone steroids early because they are immunosuppressants and reduce the body's ability to combat the virus. You give people steroids when there is a risk of excessive immune system activity. So, if HCQ were any use against cytokine storm, it would also work with later administration for more severe symptoms. But it doesn't work, so it doesn't work.Giving HCQ AFTER the cytokine storm caused ARDS is proof it doesn't help with said cytokine storm? How does that make any sense?
And yet they don't work to treat covid-19. It is not unusual to find that drugs that theoretically should be beneficial by some mechanism of action are not in practice.Moreover, both CQ and HCQ have been proven to have immunomodulatory activities by interfering with Toll-like receptor signaling pathways, reducing cytokine production, and inhibiting MHC class II expression, antigen presentation, and immune activation through the reduction of CD154 expression in T cells.
Yeah, and they don't help your case, either.Meta-analysis of non-significant results can equal significant results.
You mean a study, which found one that could be safely identified as outside transmission. But when you think about what that actually means, it means approximately sod all. It's like arguing that there are no burglaries that occur except for those where the burglar was caught and convicted. It was also apparently conducted when the Chinese government had substantially banned outdoors gatherings. Mm.The studies that trace by 7,000+ transmissions only find a small handful from outdoors does not come close to equaling even 1% let alone 5-10%. I recall you not liking estimations when IFRs came into play.
There are in fact about half a dozen or more looking at outdoors transmission. They're clocking in about 5-10% of cases. (Of course, contextually, most people without outdoors jobs also spend about 90% of their time indoors, too). There are statistics suggesting that places which allowed mass outdoor gatherings (e.g. sports events) were associated with bursts of subsequent infections. You can add to this earlier studies conducted on other respiratory diseases, which are broadly consistent for showing evidence of outdoors transmission as a significant minority.
That is not a scientifically-derived conclusion.Like I said, you just don't invade people's personal spaces and your pretty much gonna be fine outside.
With absolutely massive caveats. Again, you need to read what you are citing more carefully, and you need a wider grasp of the literature. If you just cherry pick something that says what you want you're only spouting so much bullshit.Meta-analysis of flu/mask studies found no significant reduction in flu via wearing masks.
Nonpharmaceutical Measures for Pandemic Influenza in Nonhealthcare Settings—Personal Protective and Environmental Measures
Pandemic Influenza—Personal Protective Measureswwwnc.cdc.gov