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Anti-inflammatory activity of ivermectin in late-stage COVID-19 may reflect activation of systemic glycine receptors
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  • Published on:
    Ivermectin May Prevent and Reverse Immunosenescence By Antagonizing Alpha-fetoprotein and Downmodulating PI3K/Akt/mTOR Hyperactivity

    In their recent discussion on the anti-inflammatory activity of ivermectin in sepsis, DiNicolantonio et al. [1] left open the question on how ivermectin may protect against COVID-19 initial symptoms and progression.

    Insight was published by Li et al. [2] in their derivation of an ivermectin host protein and SARS-CoV-2 host protein interaction network (PPI). For this they metabolically labelled proteins in an ovarian cancer cell line and determined which proteins were upregulated and downregulated related to a 24 hour exposure to ivermectin versus no exposure. There were 4,447 identified proteins differentially regulated by ivermectin. When compared with the 284 host proteins known to be affected by SARS-CoV-2, this left 52 proteins in common, 50 of which were downmodulated. Only two proteins, HMOX1 and IL1F10 were upregulated by ivermectin.

    This protein-protein interaction (PPI) network revealed EGFR at the center of the pathway with connections to mTOR/APOE, NFKB1/APP, AKT, MAPK1, and CASP3 through TGFB1 interacting with the protein ALB (albumin). BSG, recently shown to be absolutely essential for foam cell formation in macrophages [3] was also captured in the PPI network. Moreover, foam cell formation has been shown in macrophages to be mediated under the direction of EGFR [4] as well as for the foamy sebocytes of sebaceous glands which line the mucosal surfaces and may be an important site of viral entry [5]. Foam cell formation is important in ho...

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    Conflict of Interest:
    None declared.