"Therefore, it is plausible that the S protein of SARS-CoV-2 might mediate potent infectivity, even on cells expressing low hACE2, which would, in turn, explain why the transmission rate of SARS-CoV-2 is so high. It is also possible that other receptors mediate the entry of SARSCoV-2 into T cells, such as CD147, present on the surface of T lymohocytes, which was recently reported to be a novel invasive
route for SARS-CoV-2. ... These results suggest that SARS-CoV-2 can also enter T lymphocytes through the receptor-mediated endocytosis pathway. "
So that's frustrating because some very loud and authoritative voices have said only ACE2 in combination with TMPRSS2 allows SARS-COV-2 to bind to and infect a cell, and these are primarily in the respiratory track.
https://www.embopress.org/doi/epdf/1.../embj.20105114
So many therefors follow... but are they off?
We know about cardiac involvement...
(I don't buy the RBC/heme destruction theory, but the lack of ACE2 binding sites is given as a reason for implausibility...)
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