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The host cell plasma and endosomal membranes are critical cellular structures that serve as the primary interface between a virus and its host [Antiviral Res., 2021]. The plasma membrane acts as the outer boundary of the cell, while endosomal membranes define internal compartments involved in the endocytic pathway [Nature Reviews Microbiology, 2013]. Many enveloped viruses, such as SARS-CoV-2 and Influenza, exploit these membranes to gain entry into the cell through fusion or endocytosis [PMID 32358203]. Drugs targeting these membranes, such as Umifenovir (Arbidol) or Docosanol, typically act by preventing the fusion of the viral envelope with the host membrane or by altering the local environment, such as pH, to inhibit viral uncoating [PubChem CID 12620, PMID 16115318]. While these membranes are essential for viral entry, they also perform vital physiological functions, making them challenging targets due to the risk of off-target effects on normal cellular processes like nutrient transport and signal transduction [PMID 33242561]. Despite these challenges, targeting the host-virus interface remains a viable strategy for developing broad-spectrum antivirals, particularly for emerging viruses where specific viral protein inhibitors are not yet available [PMID 32358203].
Inhibition of viral-host membrane fusion and alteration of the endosomal environment.
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