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Disulfiram (DSF), an FDA-approved therapeutic agent for alcohol dependence, has recently attracted considerable interest due to its broad-spectrum inhibitory effects against various viruses. Increasing evidence suggests that DSF can inhibit viral replication through two major mechanisms: the inhibition of viral protein catalytic activity and the ejection of Zn from viral proteins. This review comprehensively summarized the molecular mechanisms underlying DSF's antiviral activity against viruses such as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), hepatitis C virus (HCV), influenza virus, human immunodeficiency virus (HIV), and Kaposi sarcoma-associated herpes virus (KSHV), with a particular focus on its dual targeting of Cys residues and Zn coordination sites.
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The therapeutic value of antiviral nucleoside analogs was highlighted during the coronavirus disease 2019 (COVID-19) pandemic, with remdesivir and molnupiravir repurposed for their broad-spectrum antiviral activity. The cytidine analog azvudine (FNC) has recently gained attention as a potential treatment for human immunodeficiency virus type 1 (HIV-1) and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Considering the distinct substrate specificities of HIV-1 reverse transcriptase (RT) and SARS-CoV-2 RNA-dependent RNA polymerase (RdRp), a unifying mechanism of inhibition remains elusive.
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