Control of mRNA stability by the virion host shutoff function of herpes simplex virus.

摘要: vhs1 is a mutant of herpes simplex virus type 1 that defective in the virion host shutoff function responsible for degradation cellular mRNAs and concomitant protein synthesis. In this study, effect mutation on metabolism viral was examined by measuring half-lives patterns accumulation 10 different representing all kinetic classes. The had dramatically lengthening cytoplasmic mRNAs. wild-type infections, similar half-lives, suggesting little, if any, target mRNA selectivity exhibited vhs function. caused overaccumulation number most dramatic alpha (immediate-early) ICP27 beta (early) encoding thymidine kinase, ICP8, DNA polymerase. Whereas infections these increased to peak levels subsequently declined abundance, they continued accumulate until late times. A significant but less observed several beta-gamma (delayed-early) gamma (late) results suggest plays an important role determining belonging classes so doing normal downregulation at times gene expression.