Quite an elegant bit of research to demonstrate di
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Most of the viral attack focuses on endothelial cells via the ACE2 receptor; with CD4 cells their research suggests a leveraging of glycoprotein attachment/stabilization on the cell surface until proximity to and subsequent binding to an ACE2 receptor on the same cell can come to fruition. I can’t comment on whether the glycoprotein the SARS COV2 virus attaches to is the CCR5 receptor but I would not assume so.
At the end of the day the virus is still taking out an important part of the immune response, not just wreaking havoc on endothelial cells which in turn triggers a cytokine response and a trafficking of immune cells to resolve the destruction left in its wake.