Enhanced survival of ultraviolet-irradiated herpes simplex virus in cells exposed to antiviral agents.
Enhanced survival of UV-irradiated HSV-1 is demonstrated in monkey cells exposed to inhibitors of viral DNA synthesis. Phosphonoacetic acid (PAA), adenine arabinoside (ara-A), and cytosine arabinoside (ara-C) pretreatment of infected cells is associated with concentration-dependent reactivation of UV-HSV-1. At concentrations that result in enhanced virus survival, inhibition of cell DNA synthesis is observed by either ara-A or ara-C, but not by PAA. Pretreatment of uninfected cells with acycloguanosine (ACG) is not associated with reactivation of irradiated HSV-1, and this is probably due to insufficient generation of ACG-triphosphate, the active inhibitor of viral and cell DNA synthesis.
D000212:Acyclovir / Q000494:pharmacology*; D000818:Animals; D002460:Cell Line; D002522:Chlorocebus aethiops; D003561:Cytarabine / Q000494:pharmacology*; D004261:DNA Replication / Q000187:drug effects / Q000528:radiation effects*; D007668:Kidney; D009943:Organophosphorus Compounds / Q000494:pharmacology*; D010746:Phosphonoacetic Acid / Q000494:pharmacology*; D018139:Simplexvirus / Q000187:drug effects / Q000235:genetics / Q000528:radiation effects*; D014466:Ultraviolet Rays; D014740:Vidarabine / Q000494:pharmacology*; D014779:Virus Replication / Q000187:drug effects / Q000528:radiation effects
D009943:Organophosphorus Compounds; D003561:Cytarabine; D014740:Vidarabine; D010746:Phosphonoacetic Acid; D000212:Acyclovir