Good article. But we found just the opposite,"

Good article.

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But we found just the opposite," Yang said. "Patients who improved were those who started with low CCR5 on their T cells, suggesting their immune system was less active than normal, and levels of CCR5 actually increased in people who improved.

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We know some viruses can downregulate CD4 T-cells (such as HIV and Covid). Blocking CCR5 with leronlimab increases CD4 cells levels to normal. With increased CD4 T-cells the opportunity for increased CCR5 expression naturally occurs.

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This leads to the new hypothesis that long COVID in some persons is related to the immune system being suppressed and not hyperactive, and that while blocking its activity, the antibody can stabilize CCR5 expression on the cell surface leading to upregulation of other immune receptors or functions.
https://www.sciencedaily.com/releases/2022/04...161536.htm

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I don't think the effect is from stabilized CCR5 expression as much as it's driven by an increase in CD4 T-cells. My hypothesis of other receptors taking up the slack when CCR5 is blocked holds true in this scenario. Other CCR receptors that bind the same ligands (CCL-5 - Rantes etc.) as CCR5 are also expressed on CD4 T-cells and would also increase when CD4 T-cells increase. Cytodyn should explain this to the FDA so they can finally figure out that yes indeed, Leronlimab is an immunomodulator.