Herpes simplex virus type 1 ICP0 regulates expression of immediate-early, early, and late genes in productively infected cells.

摘要: The herpes simplex virus type 1 protein, ICP0, can activate expression of all kinetic classes viral promoters in transient assays. To examine the role ICP0 regulation gene during productive infection, we characterized wild-type virus, an null mutant (7134), and several nonsense viruses with regard to replication protein synthesis Vero cells. Relative 7134 was severely deficient growth at low multiplicities infection but exhibited a nearly phenotype high multiplicities. phenotypes mutants were intermediate between those that more ICP0-coding sequence expressed by given mutant, wild type-like its phenotype. location domain responsible for transactivation confirmed be within N-terminal portion as previously shown Immunoprecipitation immunofluorescence tests used detect low-level selected immediate-early (IE), early (E), late (L) proteins following low-multiplicity infection. deletion markedly reduced levels E L IE ICP4. Because latency-associated transcripts (LATs) are specified strand opposite which encodes definition ICP0-LAT double mutants. ability LAT- ICP0+ replicate efficiently ICP0-expressing 0-28 cells complement defects indicates caused mutations not LATs. Thus, conclude up-regulates necessarily activation is likely overshadowed activity virion-associated VP16. This hypothesis tested transfection infectious DNAs. In such tests, no VP16 present times posttransfection. Significantly fewer transfected DNA ICP4 than KOS DNA. reduction fully reversed cotransfection plasmid.(ABSTRACT TRUNCATED AT 400 WORDS)