THE ROLE OF THE GENE-71 PRODUCT IN THE LIFE-CYCLE OF EQUINE HERPESVIRUS-1

Equine herpesvirus type 1 (EHV-1) gene 71 encodes a heavily O-glycosyl ated 192 kDa protein with no identified herpesvirus homologue. Isolati on of a deletion mutant in gene 71 (ED71) demonstrated that its protei n product is not essential in vitro. To investigate the role of the ge ne 71 protein in the virus life cycle, ED71 has been characterized in vitro in terms of cellular adsorption, penetration, egress and transmi ssion compared to wildtype and revertant virus. ED71 virions adsorbed to cells less efficiently than wild-type and revertant virus with a co nsequential effect on virus penetration; virus egress was significantl y impaired and the timing of release was also delayed. The percentage of both full and empty capsids accumulating in the nuclei of ED71-infe cted cells was significantly higher than in wild-type virus-infected c ells but the most notable differences were the low number of particles and the low ratio of enveloped to unenveloped capsids in the cytoplas m. The primary mode of transmission of the mutant virus is by direct c ell-to-cell spread and the fact that a neutralizing antiserum did not reduce ED71 plaque size, supported the conclusion that deletion of gen e 71 impairs the ability of virus to spread via release and readsorpti on to uninfected cells. Thus, deletion of EHV-1 gene 71 results in a d efect in virus maturation and capsid envelopment. Progeny virus is con sequently impaired in adsorption/penetration presumably due to the par ticles lacking the glycoprotein spikes predicted to be encoded by this gene and hence spreads by direct cell-to-cell contact.