I saw a few articles lately that speak to this. I am sorry I can%u2019t cite them. I believe both were in the NYTimes.
1. There is evidence that Covid got to the US much sooner than previously thought as in November December of 2019.
The earliest hard evidence is
deaths in northern California on 6 and 17 February, confirmed by retrospective tests which found "SARS2 virus" - presumably genetic material. On average it's about 27 days from infection to death so that suggests infection around the 10 and 21 January give or take a week or so. Since by February they were testing people who had travelled to Wuhan, that suggests we can be pretty sure there was community transmission in Northern California by early January.
Previously the earliest US death had been thought to be
one in Seattle on 26 February (ie infected around 30 January) and the first confirmed test was on 19 January. There may well have been the odd one missed in February but given that there are direct flights from Wuhan to San Francisco you'd expect the Bay Area to be one of the first places it would show up. We can assume that the kind of people making 12 hour flights across the Pacific are younger and not typically in high-risk groups, but on the other hand Christmas is a perfect time for super-spreader events - lots of people crowding indoors, lots of hugging and singing, lots of interaction between younger people and the elderly etc.
Even with that in mind, from what we now know about death rates you'd be surprised if none of the first 100 infectees died, so if the first death really was 6 February then that suggests there were <100 infectees in the US as of ~10 January - and potentially as few as 10 or so if they were all old. So we're talking well within the scope of a single superspreader event - or perhaps more likely some circulation for a couple of weeks - but not months - before 10 January. So you can explain the observed death rates with just one infectee coming from Wuhan to San Francisco just before Christmas last year, maybe a US businessman coming back from a business trip, or someone coming from Wuhan to see family over Christmas.
So one doesn't need infections long before Christmas to explain the observed deaths - whereas if you are claiming a lot of infection well before Christmas then you need to demonstrate increased deaths which we don't see. Yes the odd one might be missed, but not the results of a widespread infection. And I suspect there's been quite a lot of testing of old samples to try and find virus in them - it's not easy to do always, but given the huge kudos of reporting something that rewrites the story then the fact that there's been no reports of virus in pre-Christmas samples suggests that it certainly wasn't common before Christmas.
Which brings us to the report I think you're talking about,
Basavaraju et al - the "antibodies in December" paper. The first thing to say is that any antibody evidence is indirect so you can never say anything definite with them - and cross-reactions are a real problem.
The second thing to say is that the authors themselves will only allow themselves the conclusion that their testing "
suggests that the virus was present in the United States earlier than previously recognized" - they're not commiting to anything definite, just a "suggestion", and not a date, just "earlier". As they themselves say "
These data might indicate that there is no clear delineation between potentially cross reactive specimens, and those that were obviously from SARS-CoV-2 infected individuals....The S1 subunit has been reported to be a more specific antigen for SARS-CoV-2 serologic diagnosis than the whole S protein"
So everyone got excited about the headline finding that 106 out of 7,389 samples had some kind of reaction with SARS2, but once you look into the detail it looks like ~56% of those were definitely cross-reactions, and just one had a reaction with SARS2 S1 subunit. So they think something's going on, but there's only one they feel really confident about :
"
Collectively, these data suggest that at least some of the reactive blood donor sera could be due to prior SARS-CoV-2 infection. One serum, collected on January 10, 2020 in Connecticut, demonstrated a neutralization titer of 320, 6.75 signal to threshold ratio, and 70% inhibition activity by surrogate neutralization activity, but was Ortho S1 non-reactive. These data indicate that this donation was likely from an individual with a past or active SARS-CoV-2 infection."
No doubt in time we'll get a better feel for which patterns of antibodies come from SARS2 and which from infection with other coronaviruses. The one that was S1 positive is interesting - a sample from a 16-29yo man from Northern California, collected 13-16 December. Which far from disproving anything, is exactly consistent with the kind of conclusion we'd drawn from the pattern of deaths - and once it gets on a direct flight from Wuhan to SFO it can readily spread through the US.
Topic: Covid19 (Read 5433 times)
