Inhibition of vesicular stomatitis virus replication by 9-beta-D-arabinofuranosyladenine.
9-beta-d-Arabinofuranosyladenine (Ara-A) effectively inhibited the production of infectious vesicular stomatitis virus (VSV) in MDBK cells. Furthermore, inhibition was shown to begin as early as the first 3 hr of infection. Studies employing (3)H-l-leucine indicated that Ara-A did not affect protein synthesis in uninfected cells, although it did cause a marked stimulation of protein synthesis in VSV-infected cells during the log phase of the growth cycle. Puromycin, an inhibitor of protein synthesis, was a more effective viral inhibitor than Ara-A. However, the combination of Ara-A and puromycin was less effective than puromycin alone except when present for long time periods. Short-term labeling experiments with (3)H-uridine demonstrated that Ara-A depressed ribonucleic acid (RNA) synthesis in uninfected cells, whereas periods of stimulation and depression of radioisotope incorporation occurred in infected cells. The results support the notion that Ara-A is incorporated into RNA early during viral replication.
D000225:Adenine / Q000494:pharmacology*; D000998:Antiviral Agents / Q000494:pharmacology*; D001089:Arabinose / Q000494:pharmacology; D005663:Furans / Q000494:pharmacology; D009705:Nucleosides / Q000494:pharmacology*; D014721:Vesicular stomatitis Indiana virus / Q000187:drug effects*; D014779:Virus Replication / Q000187:drug effects*
D000998:Antiviral Agents; D005663:Furans; D009705:Nucleosides; D001089:Arabinose; D000225:Adenine