More things I've learned about Covid-19

It's been a while since the last two posts on the topic so it seemed like a good idea to write down what I'd learned or changed my mind about recently on the topic.

Immunity changes symptom timing

One thing that's become important in the Omicron wave is that it seems that if you train your immune system to recognize a disease then you'll develop symptoms of that disease more quickly than if your body doesn't recognize it.  Most of the symptoms we tend to get when sick like inflammation or a fever aren't directly caused by the disease but by our body's innate immune system fighting it.  I'm actually not sure exactly why adaptive immunity leads to triggering innate immune responses faster but it's apparently a thing.  Michael Mina has a nice infographic here on the topic which is also arguing that this means waiting 5 days after symptom onset to return to work might now not be good enough when previously it would have been.

Previously the one genuinely weird thing you could point to about SARS-CoV-2 was that people didn't start developing symptoms until their viral load had peaked, making it much harder to stop transmission than other diseases.  But if this is going away with previous exposure how unique is it really?  If one of the four common cold coronaviruses worked this way would we expect to have identified this prorperty?  Nobody is going around taking the viral load of kids getting their first cold, after all, and the symptoms seem to be relatively mild for them just as for the common cold.  So I'm no longer sure this aspect of SARS-2 is out of the ordinary.

Upper and lower

One thing about Covid-19 was that I started to distinguish upper respiratory infections 

which spread more by droplets than aerosols and which often involved fomite transfer versus lower respiratory infections which were mostly about aerosols and which didn't involve fomites very much.

The former would involve most flu and most common colds while the later would include SARS-Cov-2, H5-N1 flu, and a few other diseases.  But I'm not sure exactly how I'd want to categorize Omicron SARS-2 and so maybe that binary classification is too simple?  Omicron still needs an ACE2 receptor to invade a cell but the original SARS-2 mostly relied on TMPRSS2b proteins to go from latched on to a cell to inside it whereas omicron seems to do a fine job entering without that extra protein. Since TMPRSS2b was common in lungs but not elsewhere in the respiratory tract that means more virus in the throat and nose and less in the lungs.  Since it's been lung damage that's mostly been killing people that's been rather welcome news overall even if high viral load higher up the respiratory tract means an easier transmission chain.  After all it's only the finer aerosols that can get deep into the lungs but its easier for larger droplets with more virus to get to a person's throat.

The question we have, though, is what to worry about.  With the original gangster SARS-2 it was mostly aerosols that were the danger but is that still true with Omicron?  Should we be more worried about six foot distancing now with droplets?  Hand washing was pretty much useless against the original SARS-2 with barely any fomite transfer but with Omicron is this something we should actually be concerned about now?  I really have no idea and intend to be a bit cautious about this.

There's also the odd case of hydroxychloroquine.  It seems to do a good job of preventing cells with ACES2 receptors but no TMPRSS2bs from being infected but of course since most transmissions in the original SARS2 involved TMPRSS2b that meant that as a drug to prevent infection it was pretty much useless. But with Omicron mostly using endosomal entry which hydroxychloroquine can actually block does that mean that hydroxychloroquine is suddenly actually a useful drug?  I hope someone does a study on this.

Future Evolution

There's nothing saying that any virus ought to intrinsically evolve to be less virulent.  Being more transmissible often invovles being less severe about one's symptoms but while SARS-2 was doing most of its transmission before symptoms started at all there was little pressure on it to be gentler on its victims.  But now that our immune systems are recognizing it earlier and starting symptoms before most transmission takes place should that actually tend to select for less deadly variants?  Maybe, it seems like.  To the extent to which bad symptoms keep people at home and not spreading their infections and that these symptoms correlate to danger to people's lives at least.  That's hardly a guarantee but I'm a lot more optimistic about this than I was a year ago mostly due to this earlier manifestation of symptoms.

Lab Leaks

Way back in 2020 I was arguing a lot that there was no reason to think that SARS-CoV-2 was an artificial virus.  Wuhan was an big crossroad of shipments across China so even if a virus like that wouldn't be native to the province it wouldn't be too odd that it would virus have large outbreak there. Another large possibility is that some researcher from the Wuhan Institute of Virology could have picked it up while exploring bat caves or that a researcher from the Chinese CDC could have acquired it while investigating an outbreak of pneumonia in some backwater Yunan village but acquired a natural infection nonetheless.

i'd almost entirely dismissed the idea that SARS-CoV-2 could have been created in a lab but this year I'm a lot less certain.  The fact that researcher from the WIV had applied to the US NIH for funding to take a coronvirus from southeast asia, add a furin cleavage site to it, and check just how dangerous the resulting virus was fills me with foreboding.  The funding was denied because at that point that sort of gain of function research as banned at the NIH due to its dangers.  But one worries that scientists might have gotten funding for the research they wanted to carry out in other ways even without NIH funding.  And this shows that adding furin cleavage sites to bat corovaviruses was very much on the agenda.  

I'd also thought that if it had been a lab leak there'd have been some sort of smoking gun as published genomes would have left a track record.  But while it was initially denied that there was any near relative of SARS-CoV-2 known to science it eventually came to light that a very similar virus previously killed people then been sampled.  The previous existence of a near relative and efforts to hide it after the Covid-19 pandemic are exactly what I thought shouldn't exist and have forced me to re-evaluate my position.  This is all rather embarrassing in light of my previous arguments but when new data comes around you have to update your positions or else you end up in absurd situations.