Transfer of UL41, the gene controlling virion-associated host cell shutoff, between different strains of herpes simplex virus.
Studies with mutant viruses have suggested that the product of gene UL41 of herpes simplex virus type 1 (HSV-1) controls the virion-mediated inhibition of cellular protein synthesis as well as the rate of degradation of viral mRNAs. HSV-1 strain 17+ has a weak host shutoff function, whereas HSV-2 strain G shuts off strongly. A gene of HSV-2(G), judged from its position in the genome to be the probable analogue of gene UL41 of HSV-1, was inserted into the nonessential thymidine kinase gene of HSV-1(17+). The recombinant virus, 17G41, exhibited a strong shutoff function and its immediate early mRNA did not accumulate in the presence of cycloheximide. It resembled HSV-2(G) in these respects and not the parent, confirming the function of the transferred gene. Recombinant virus 17G41 carries the UL41 genes of both strains, 17+ and G, and in this situation the strong shutoff function was dominant. However, after mixed infection with equal multiplicities of 17G41 and HSV-1(17+) the weak shutoff function was dominant. The recombinant, 17G41, was further modified by insertion of a lacZ expression cassette into the coding region of the original gene UL41 (17+). The resulting virus, 17(41-)G41, also had a strong shutoff activity but grew poorly in tissue culture.
Fenwick
M L
ML
Sir William Dunn School of Pathology, University of Oxford, U.K.
Everett
R D
RD
D000818:Animals; D015139:Blotting, Southern; D002460:Cell Line; D004279:DNA, Viral / Q000235:genetics; D005814:Genes, Viral; D010957:Plasmids; D014176:Protein Biosynthesis; D012333:RNA, Messenger / Q000378:metabolism; D012367:RNA, Viral / Q000378:metabolism; D018139:Simplexvirus / Q000235:genetics* / Q000502:physiology; D013937:Thymidine Kinase / Q000235:genetics; D014162:Transfection; D014771:Virion / Q000235:genetics / Q000502:physiology
D004279:DNA, Viral; D012333:RNA, Messenger; D012367:RNA, Viral; D013937:Thymidine Kinase