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What a coincidence
“The binding epitope on S harbors a sequence motif unique to SARS-CoV-2 (not present in other SARS-related coronaviruses), which is highly similar in both sequence and structure to the bacterial superantigen staphylococcal enterotoxin B”
https://www.pnas.org/content/117/41/25254
“The binding epitope on S harbors a sequence motif unique to SARS-CoV-2 (not present in other SARS-related coronaviruses), which is highly similar in both sequence and structure to the bacterial superantigen staphylococcal enterotoxin B”
https://www.pnas.org/content/117/41/25254
Now, this story keeps unfolding.
“the trimeric spike protein of SARS-CoV-2 could bind to TLR4 directly and robustly activate downstream signaling in monocytes and neutrophils.” Via MyD88 and NFκB https://twitter.com/biorxiv_immuno/status/1340118645624729600?s=21
“the trimeric spike protein of SARS-CoV-2 could bind to TLR4 directly and robustly activate downstream signaling in monocytes and neutrophils.” Via MyD88 and NFκB https://twitter.com/biorxiv_immuno/status/1340118645624729600?s=21
See how MyD88 activation is THE problematic pathway, especially when amplified by elevated LPS exposure. I.e. by metabolic diseases.
How the two pathways join at this signaling node
https://journals.sagepub.com/doi/10.1177/1753425910374092
How the two pathways join at this signaling node
https://journals.sagepub.com/doi/10.1177/1753425910374092
“the most profound disturbances including a prominent neutrophil hyperactivation signature and monocytes with anti-inflammatory features. We further demonstrate that emergency myelopoiesis is a prominent feature of fatal COVID-19.”
Monocytes featuring trained innate immunity? https://twitter.com/biorxiv_immuno/status/1340088358203211777
Monocytes featuring trained innate immunity? https://twitter.com/biorxiv_immuno/status/1340088358203211777
