Characterization of an herpes simplex virus type 2 mutant, which is resistant to acycloguanosine and causes fusion of BSC1 cells.
A mutant of herpes simplex virus type 2, which induces low levels of thymidine-kinase activity in infected BSC1 cells and consequently able to grow in the presence of acycloguanosine, was isolated. This mutant has also been shown to cause fusion of BSC1 cells. In BSC1 cells, co-infected with the wild-type strain and the mutant, the yield of each of the two viruses was normal but the rounding and aggregation of cells observed, resembled that found in wild-type infected cultures. When the mixed infection was performed in the presence of acycloguanosine (100 micrometers), the growth of the two virus strains was inhibited, as well as the cytopathic effect in the cultures. It is suggested that under these conditions, the thymidine-kinase which was induced in the infected cells by the wild-type strain, phosphorylated acycloguanosine and the activated drug formed, inhibited the growth of the two viruses by interference in their DNA syntheses.
D000212:Acyclovir / Q000494:pharmacology*; D000818:Animals; D002459:Cell Fusion; D002460:Cell Line; D002522:Chlorocebus aethiops; D004259:DNA-Directed DNA Polymerase / Q000378:metabolism; D004352:Drug Resistance, Microbial; D009154:Mutation; D010746:Phosphonoacetic Acid / Q000494:pharmacology; D018139:Simplexvirus / Q000187:drug effects / Q000235:genetics / Q000502:physiology*; D013937:Thymidine Kinase; D014764:Viral Proteins / Q000032:analysis
D014764:Viral Proteins; D013937:Thymidine Kinase; D004259:DNA-Directed DNA Polymerase; D010746:Phosphonoacetic Acid; D000212:Acyclovir