Abstract
Amantadine has been known to be a potent inhibitor of influenza A virus infection for many years (1). Although amantadine’s antiviral effect on many other viruses is much less potent that observed for influenza A, it does have a fairly broad antiviral spectrum (2,3). The extreme sensitivity of influenza A virus to the drug has been shown by genetic and molecular biologic studies to reside with the M2 protein. Amantadine interacts with M2 and inhibits its ability to function as a pH-gated ion channel, and thus appears to interfere with a step in influenza virus uncoating and assembly (4–6). Amantadine exerts its more broad-spectrum antiviral effects by virtue of its lysomotropic properties. The drug accumulates in endocytic vesicles, raises their pH, and thus interferes with the ability of viruses requiring low pH to complete uncoating and penetration from entering the cytosol (2,3).
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Leibowitz, J.L., Reneker, S.J. (1994). The Effect of Amantadine on Mouse Hepatitis Virus Replication. In: Laude, H., Vautherot, JF. (eds) Coronaviruses. Advances in Experimental Medicine and Biology, vol 342. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-2996-5_19
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DOI: https://doi.org/10.1007/978-1-4615-2996-5_19
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