SA, your comments on those papers are entirely appropriate. Yes, some of this is very vague data. Yes, it would be immensely time consuming for any individual, but thankfully there is a vast scientific community looking into all these preliminary studies.
But the process takes time, whereas probably the most certain thing about SARS-CoV-2 is that it can spread extremely fast. And it’s mutating, diversifying, and every additional infected person gives it more opportunities to do so.
Hence my frustration with those who argue against all and any measures to slow the damn thing down. Far better to take precautions now, show some patience and self restraint, such that we’re in a much better position if SARS-CoV-2 does spring some nasty surprises upon us in the coming months. Surprises like these:
Superantigenic character of an insert unique to SARS-CoV-2 spike supported by skewed TCR repertoire in patients with hyperinflammation
PNAS October 13, 2020 117 (41) 25254-25262; first published September 28, 2020
– A hyperinflammatory syndrome reminiscent of toxic shock syndrome (TSS) is observed in severe COVID-19 patients, including children with Multisystem Inflammatory Syndrome in Children (MIS-C). TSS is typically caused by pathogenic superantigens stimulating excessive activation of the adaptive immune system. We show that SARS-CoV-2 spike contains sequence and structure motifs highly similar to those of a bacterial superantigen and may directly bind T cell receptors. We further report a skewed T cell receptor repertoire in COVID-19 patients with severe hyperinflammation, in support of such a superantigenic effect. Notably, the superantigen-like motif is not present in other SARS family coronaviruses, which may explain the unique potential for SARS-CoV-2 to cause both MIS-C and the cytokine storm observed in adult COVID-19.
SARS-CoV-2 Uses CD4 to Infect T Helper Lymphocytes
doi.org/10.1101/2020.09.25.20200329
– The mechanism by which SARS-CoV-2 infection may result in immune system dysfunction is not fully understood. Here we show that SARS-CoV-2 infects human CD4+ T helper cells, but not CD8+ T cells, and is present in blood and bronchoalveolar lavage T helper cells of severe COVID-19 patients. We demonstrated that SARS-CoV-2 spike glycoprotein (S) directly binds to the CD4 molecule, which in turn mediates the entry of SARS- CoV-2 in T helper cells in a mechanism that also requires ACE2 and TMPRSS2. Once inside T helper cells, SARS-CoV-2 assembles viral factories, impairs cell function and may cause cell death. SARS-CoV-2 infected T helper cells express higher amounts of IL-10, which is associated with viral persistence and disease severity. Thus, CD4-mediated SARS-CoV-2 infection of T helper cells may explain the poor adaptive immune response of many COVID- 19 patients.