An analysis of the in vitro and in vivo phenotypes of mutants of herpes simplex virus type 1 lacking glycoproteins gG, gE, gI or the putative gJ.

摘要: Mutants of herpes simplex virus type 1 (HSV-1) lacking glycoproteins gG, gE, gI or the putative gJ were constructed by inserting a lacZ expression cassette within US4, US8, US7 and US5 genes respectively. Revertant viruses then rescue with wild-type DNA fragment. Each these mutant viruses, comparison parental HSV-1 SC16, exhibited normal particle to infectivity ratios, had no discernible phenotypic abnormalities in baby hamster kidney-21 cells following high low multiplicity infections. Infection mice scarification ear showed following. (i) Interruption (gJ) gene has effect on ability multiply at inoculation site its enter peripheral central nervous system (CNS). This shows that provides convenient for insertion foreign both vitro vivo studies. (ii) Disruption US4 (gG) results marginal attenuation mouse model. (iii) (gI) US8 (gE) pronounced attenuation; was rapidly cleared from barely detectable sensory ganglia CNS. The failure gI-negative gE-negative replicate efficiently led investigation behaviour epithelial vitro. Viruses gE adsorbed entered rates compared virus, but formed minute plaques. is consistent cell-to-cell spread cell contact route. confirmed measurement rate increase infectious centre numbers view influence interactions between plasma membrane reinforced showing introduction disrupted into syncytial, otherwise syngeneic, background resulted non-syncytial phenotype. We conclude gE-gI complex plays part, least some types, surface allow transmission infected uninfected contact. In syncytial strains this leads uncontrolled fusion. observation virions apparently reinforces cell-cell fusion not analogous virion envelope nucleocapsid entry. It also apparent phenotypes mutants are similar many respects those reported pseudorabies homologue.