Verapamil inhibits influenza A virus replication.
Calcium channel blockers reduce Ca++ flux through membrane channels and may inhibit intracellular Ca++-dependent synthetic and regulatory activities by binding to calmodulin. We have found that Verapamil, a calcium channel blocker, inhibits influenza virus replication in Madin-Darby canine kidney cells and in murine pulmonary macrophages and that this antiviral effect occurs with drug addition late in the replication cycle. Chlorpromazine, a drug which binds to calmodulin, also inhibited influenza virus replication in these tissue culture systems. We suggest that Verapamil and chlorpromazine inhibit influenza virus replication by interfering with calmodulin-dependent intracellular activities necessary for late synthetic steps or virus assembly steps and that calcium channel blockers provide a new probe for investigating influenza virus replication.
D000818:Animals; D002460:Cell Line; D002478:Cells, Cultured; D004261:DNA Replication / Q000187:drug effects*; D004285:Dogs; D009980:Influenza A virus / Q000187:drug effects / Q000235:genetics*; D007668:Kidney; D007700:Kinetics; D051379:Mice; D014700:Verapamil / Q000633:toxicity*; D014779:Virus Replication / Q000187:drug effects
D014700:Verapamil