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The hypothesis is that hydroxychloroquin interferes with glycosylation of cell surface proteins that are essential for entry of the virus into the cell. The zin
by HarryHirsch 7y ago
The hypothesis is that hydroxychloroquin interferes with glycosylation of cell surface proteins that are essential for entry of the virus into the cell. The zinc notion is total bunk, intracellular zinc concentration is tightly controlled. Random zinc excursions just don't happen, if they did they would result in death.
- podgaj 7y agoThis is so wrong I do not know where to start. ADAM17 is responsible for shedding of ACE2 from the cell which creates soluble ACE2. If ACE2 is not ON the cell the virus cannot infect the cell. ADAM17, like ACE2 is a zinc finger protein and uses zinc as a cofactor. Also, zinc is widely understood to lower the immune response by affecting interferon levels. It is not only about intracellular zinc. But in a deficiency intracellular zinc has even less chance of being brought into the cell, right? To say that zinc does not matter because hydroxychloroquin is absurd.
- giardini 7y agoHarryHirsch says "The zinc notion is total bunk..." I am unclear what you mean here but this in-vitro experiment. which studied interaction of zinc ions with chloroquine in a human ovarian cancer cell line. shows far more zinc entering cells that are exposed to chloroquine: "Chloroquine Is a Zinc Ionophore": https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4182877/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4182877/