4 ms·
I posited not that sars-1 caused some of that immunity, but that another coronavirus which was spreading around later in 2019. I lost my sense of smell complete
by subsubzero 6y ago
I posited not that sars-1 caused some of that immunity, but that another coronavirus which was spreading around later in 2019. I lost my sense of smell completely around thanksgiving 2019 and don't think that was covid-19 but a similar virus that possibly turned more deadly due to a mutation. My brother was in China earlier in October 19' and I believe he got me sick with it. He himself got sick back to back to back from whatever he had(and he never gets sick). But this is total conjecture.
- dwd 6y agoMaybe conjecture, but they are little pieces of information that seem to be common across many parts of the world at that time. The summer 2019/20 spike in hospitalised pneumonia cases in the southern hemisphere that were a non-flu virus is another data point out there - someone just needs to put them all together.
- lamontcg 6y agoWe can rule out anything other than cryptic spread in the US in 2019: https://threadreaderapp.com/thread/1249414291297464321.html https://threadreaderapp.com/thread/1249414291297464321.html https://www.nejm.org/doi/full/10.1056/NEJMc2008646 https://www.nejm.org/doi/full/10.1056/NEJMc2008646 The viruses going around 19/20 winter in WA included all kinds of non-flu viruses. The rapid flu test also suffers from the same 50% false negative rate that the rapid COVID test suffers from.
- lamontcg 6y agoSARS-CoV-2 was almost certainly spreading in Wuhan in October. If your brother was there, and caught a virus, and gave it to you, and you substantially lost your sense of smell, then you should buy a lottery ticket because you were one of a small set of cryptic 2019 infections in the US (or wherever you are). I would normally kind of shit all over anyone outside of China claiming to have caught the virus in 2019, but you tick off the two boxes which are complete and total loss of smell and contact tracing to someone actually back in China. Presumably you didn't pass it on to anyone or it otherwise died out and never found a superspreader (the majority of chains of infections of SARS-CoV-2 actually die out due to the way it transmits mostly by superspreading and it can take 4+ "seeds" on average before epidemic spread kicks off in an area).
- aitchnyu 6y agoWhy didnt we test peoples breaths for being potential superspreaders? If the vaccines make people less infectious, superspreaders should have it first. In a privacy preserving way, they should also be advised to avoid gatherings.
- lamontcg 6y agosuperspreading is probably a mix of biology and behavior and we don't even know what the biology is.
- Izkata 6y agoYou may want to reconsider that stance: https://www.redcross.org/about-us/news-and-events/press-release/2020/study-suggests-possible-new-covid-19-timeline-in-the-us.html https://www.redcross.org/about-us/news-and-events/press-rele... > The findings of this study indicate that that it is possible the virus that causes COVID-19 may have been present in California, Oregon, and Washington as early as Dec. 13-16, 2019, and in Connecticut, Iowa, Massachusetts, Michigan, Rhode Island, and Wisconsin as early as Dec. 30, 2019 - Jan. 17, 2020.
- lamontcg 6y agoYou may want to read that study closer. Most of it is finding cross reactive antibodies, which as the title study here indicates we know isn't indication of prior SARS-CoV-2 infection. Specifically this paragraph: > In order to better characterize the specimens that were reactive on the pan-Ig ELISA containing whole SARS-CoV-2 spike protein as the capture antigen, and distinguish these from cross-reactivity to common coronaviruses, additional, more specific SARS-CoV-2 testing was performed. The S1 subunit has been reported to be a more specific antigen for SARS-CoV-2 serologic diagnosis than the whole S protein [23]. Furthermore, in recent studies, sera from patients with confirmed human coronavirus infection only contained SARS-CoV-2 S protein–specific IgG antibodies and did not contain IgM or IgA antibodies; neutralizing activity in these sera was found to target only the S2 portion of the spike protein [23, 24]. Therefore, the presence of IgM or IgA antibodies and S1-specific binding activity may distinguish antibodies to SARS-CoV-2 from antibodies to human common coronaviruses [23, 24]. In the present study, 84 of 90 (>93%) reactive sera had neutralizing activity against SARS-CoV-2 virus, 39 (44.3%) had both IgG and IgM SARS-CoV-2 S protein–specific antibodies, 2 (2.2%) sera had surrogate neutralization activities, and 1 of 90 (1.1%) had SARS-CoV-2 S1-specific Ig. 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 sample, collected on 10 January 2020 in Connecticut, demonstrated a neutralization titer of 320, a signal-to-threshold ratio of 6.75, and 70% inhibition activity by surrogate neutralization activity, but was Ortho S1 nonreactive. These data indicate that this donation was likely from an individual with a past or active SARS-CoV-2 infection. They found maybe two good signals for SARS-CoV-2 infection, with only one in Jan 2020 that really passes the test for definitively being SARS-CoV-2 infection. The neutralizing titers were in the total absence of IgG/IgM SARS-CoV-2 S-protein specific antibodies, which can be cross reactivity to antibodies against other coronaviruses. The fact that they were neutralizing against SARS-CoV-2 though in vitro doesn't necessarily confer actual protection as was seen in the study that Derek Lowe cites. That study is still consistent with not knowing of any SARS-CoV-2 infections in the USA in 2019 and there being nothing possible other than cryptic spread.