Inhibition of vesicular stomatitis virus by kethoxal bis (thiosemicarbazone).
Kethoxal bis (thiosemicarbazone) (KTS) inhibited replication of, and plaque formation by, vesicular stomatitis virus (VSV) in chick embryo cells. No other thiosemicarbazones tested were effective. Virus-specific m-RNA and protein synthesis were inhibited by KTS. However, virion RNA-dependent RNA synthesis was not inhibited by the drug. Treatment of VSV virions directly with KTS produced enhancement, rather than inactivation, of plaque formation. KTS inhibited cellular DNA and RNA synthesis by 67 and 25% respectively. Since cellular DNA and RNA synthesis are not required for VSV replication, the inhibition of these processes is probably unrelated to the antivirial activity of KTS. Cellular protein synthesis was inhibited 24% by KTS. Unexpectedly, synthesis of four proteins was induced in KTS-treated uninfected cells.
D000818:Animals; D002455:Cell Division / Q000187:drug effects; D002460:Cell Line; D002642:Chick Embryo; D012321:DNA-Directed RNA Polymerases / Q000378:metabolism; D003609:Dactinomycin / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D012333:RNA, Messenger / Q000096:biosynthesis; D012367:RNA, Viral / Q000096:biosynthesis; D013882:Thiosemicarbazones / Q000494:pharmacology*; D014721:Vesicular stomatitis Indiana virus / Q000187:drug effects* / Q000254:growth & development / Q000378:metabolism; D014764:Viral Proteins / Q000096:biosynthesis; D014779:Virus Replication / Q000187:drug effects
D012333:RNA, Messenger; D012367:RNA, Viral; D013882:Thiosemicarbazones; D014764:Viral Proteins; D003609:Dactinomycin; D012321:DNA-Directed RNA Polymerases