It's just the flu!
#781
Quick solution...
Give everybody a coronavirus cold.
https://medicalxpress.com/news/2020-...es-immune.html
There are four human coronavirus strains that have been identified for decades that rarely cause even hospitalization. Yes, they’ve caused a few pneumonia’s in people who are immune suppressed, but that’s been both rare and generally survivable. Millions of person case years experience is far better than any phase 3 study.
https://medicalxpress.com/news/2020-...es-immune.html
There are four human coronavirus strains that have been identified for decades that rarely cause even hospitalization. Yes, they’ve caused a few pneumonia’s in people who are immune suppressed, but that’s been both rare and generally survivable. Millions of person case years experience is far better than any phase 3 study.
#782
https://www.the-scientist.com/news-opinion/does-the-common-cold-protect-you-from-covid-19--67792
https://science.sciencemag.org/content/early/2020/08/04/science.abd3871
https://rclutz.wordpress.com/2020/07...-from-t-cells/
https://science.sciencemag.org/content/early/2020/08/04/science.abd3871
Abstract
Many unknowns exist about human immune responses to the SARS-CoV-2 virus. SARS-CoV-2 reactive CD4+ T cells have been reported in unexposed individuals, suggesting pre-existing cross-reactive T cell memory in 20-50% of people. However, the source of those T cells has been speculative. Using human blood samples derived before the SARS-CoV-2 virus was discovered in 2019, we mapped 142 T cell epitopes across the SARS-CoV-2 genome to facilitate precise interrogation of the SARS-CoV-2-specific CD4+ T cell repertoire. We demonstrate a range of pre-existing memory CD4+ T cells that are cross-reactive with comparable affinity to SARS-CoV-2 and the common cold coronaviruses HCoV-OC43, HCoV-229E, HCoV-NL63, or HCoV-HKU1. Thus, variegated T cell memory to coronaviruses that cause the common cold may underlie at least some of the extensive heterogeneity observed in COVID-19 disease.
In light of the recent emergence of SARS-CoV-2, our data raise the intriguing possibility that such pre-existing S-reactive T cells represent cross-reactive clones, probably acquired in previous infections with endemic HCoVs. HCoVs account for approximately 20% of “common cold” upper respiratory tract infections, are ubiquitous, but display a winter seasonality30–32. Based on epidemiological data, it may be extrapolated that adults contract an HCoV infection on average every two to three years. Protective antibodies may wane mid-term but cellular immunity could remain13,33. Although the overall amino acid sequence homology of S is relatively low compared to spike glycoproteins of HCoVs, there is an overlap of MHC-II epitopes especially in the C-terminal domain of the here used peptide pools (Fig. 1a, Extended Data Fig. 1). This may explain the preferential reactivity of CD4+ T cells to the C-terminal domain in one third of HD.
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