A herpes simplex virus type 1 mutant lacking the ICP0 introns reactivates with normal efficiency.
Previous evidence suggests that the latency-associated transcript (LAT) gene of herpes simplex virus type 1 appears to have a role during reactivation of latent virus because viruses which are null mutants in this gene reactivate slowly or less efficiently than wild-type viruses. Mapping studies have shown that the LAT gene covers a region of about 8.5 kb that overlaps the ICP0 gene in the repeat long region of the herpes simplex virus genome. Previously, we had constructed a mutant with a deletion in the region of the LAT gene encoding a stable 2-kb RNA species (that accumulates to high levels in latently infected cells) and had shown that it reactivates normally (T.M. Block, J.G. Spivack, I. Steiner, S. Deshmane, M.T. McIntosh, R.P. Lirette, and N.W. Fraser, J. Virol. 64:3417-3426, 1990). We now show that a mutant which has two deletions downstream of this region (deleted in both ICP0 introns) reactivates normally in explant cocultivation assays. Thus, the slow or inefficient reactivation phenotype of herpes simplex virus type 1 LAT null mutants is not assignable to this region of the LAT gene.