Mutant of herpes simplex virus type 2 with temperature-sensitive lesions affecting virion thermostability and DNase activity: identification of the lethal mutation and physical mapping of the nuc-lesion.
We had previously shown that a temperature-sensitive (ts) mutant of herpes simplex virus type 2 strain HG52, ts13, induced a heat-labile DNase activity in infected cells (B. Francke, H. Moss, M. C. Timbury, and J. Hay, J. Virol. 26:209-213, 1978). Earlier work indicated that the mutant also possessed temperature-sensitive infectivity (I. W. Halliburton and M. C. Timbury, J. Gen. Virol. 30:207-221, 1976). In this study temperature-stable revertants of ts13 have been isolated; examination of them revealed that ts13 is a double mutant, with genetically distinct temperature-sensitive lesions affecting nuclease activity and particle stability. The lethal mutation, in the cell system studied, is the latter. Revertants, which all maintain the nuclease lesion, grew well at a high temperature. Physical mapping of the nuclease lesion placed it between 0.12 and 0.21 (fractional length) on the virus genome, quite distant from the lethal mutation at 0.64 to 0.70.
D000818:Animals; D002460:Cell Line; D006224:Cricetinae; D004262:DNA Restriction Enzymes / Q000378:metabolism; D004279:DNA, Viral / Q000032:analysis; D003851:Deoxyribonucleases / Q000235:genetics*; D005814:Genes, Viral; D007668:Kidney; D009154:Mutation; D018139:Simplexvirus / Q000032:analysis / Q000235:genetics* / Q000254:growth & development; D013696:Temperature; D014779:Virus Replication
D004279:DNA, Viral; D003851:Deoxyribonucleases; D004262:DNA Restriction Enzymes