Ultraviolet irradiation of herpes simplex virus (type 1): delayed transcription and comparative sensitivites of virus functions.
The delay in the replication of herpes simplex virus surviving u.v. irradiation occurs after the uncoating of virus, as judged by sensitivity to DNase. It occurs before translation, judged by the kinetics of appearance of various virus-specific proteins, and before transcription, judged by the detection of virus-specific RNA by in situ hybridization. Since the delays in both transcription and translation are reversed by photoreactivation, the simplest hypothesis is that pyrimidine dimers directly obstruct transcription;unless these are broken by photoreactivating enzymes, there will be transcriptional delay until reactivating processes have repaired the lesion. The u.v. sensitivities of the abilities to induce various enzymes (thymidine kinase, DNase and DNA polymerase) were only about four times less than that of infectivity. The The ability to induce the three enzymes was three times less sensitive than that of the structural antigen (Band II).
D004790:Enzyme Induction / Q000528:radiation effects; D014176:Protein Biosynthesis / Q000528:radiation effects; D018139:Simplexvirus / Q000235:genetics / Q000378:metabolism / Q000528:radiation effects*; D014158:Transcription, Genetic / Q000528:radiation effects*; D014466:Ultraviolet Rays; D014764:Viral Proteins / Q000096:biosynthesis*
D014764:Viral Proteins