SARS-CoV-2 infects human CD4+ T helper cells by binding its spike glycoprotein to the CD4 molecule, impairing cell function and potentially causing cell death.
This mechanism involves the interaction of the virus with both CD4 and ACE2 receptors.
SARS-CoV-2 infects human CD4+ T helper cells by binding its spike glycoprotein to the CD4 molecule, impairing cell function and potentially causing cell death.
This mechanism involves the interaction of the virus with both CD4 and ACE2 receptors.
This is why there are so many pathogens repeatedly circulating in ways we didn’t see before Covid.
Immune systems can’t fight off the bugs because SarsCov2 damages the immune system.
“COVID-19 leads to considerable long-term changes in the immune system, even in mild cases. The findings could help to better understand the long-term consequences of an infection with SARS-CoV-2.”
COVID-19 rapidly increases senescent and exhausted T cells, particularly CD4 and CD8 T cells.
Both mild and severe COVID-19 cases showed increased markers of T-cell exhaustion and senescence with more pronounced changes in severe cases.
Your immune system is a factory 🧵
T-cells are the essential workers.
SARS-CoV-2 -19 is a hacker that doesn't just disrupt operations from the outside.
It infiltrates the system and systematically lays off the workers (T-cells).