Major histocompatibility complex (MHC) deficiency is typical of almost all resident cells in normal neural tissue. Phosphonoacetic acid and 9-β-d-arabinofuranosyladenine blocked reactivation, but this treatment did not eradicate the latent infection. Here, it is shown that granzyme A restricts the interneuronal spread of HSV and significantly influences ganglionic virus load. LAT was not detected with probes from DNA outside the limits of the larger species. In contrast, the amount of latency-associated transcripts was much less variable, at an average of 4 x 10(4) molecules per viral genome. MCMV was produced spontaneously after 12-18 d from spleen explant cultures of 33 of 34 mice. By comparison, all the animals treated with DHPG starting at 24 h or with saline became infected.
A 3-week DHPG regimen starting 5 weeks postinfection reduced the number of animals that developed recrudescent lesions by 70%. When treatment ended, however, recrudescent episodes in the animals increased to the level of saline-treated controls.These results suggest that (i) DHPG is highly effective in reducing the severity of both primary and recrudescent lesions of herpes simplex virus type 2, (ii) early treatment of a primary infection or treatment of recrudescences reduces the incidence of recrudescences, and (iii) the drug appears to have no effect on the latent form of the virus, as the incidence of recrudescences increases when DHPG treatment is ended. Full text Full text is available as a scanned copy of the original print version. Desai, J. We conclude that explant reactivation may provide an ancillary system for selected studies of the early events in reactivation.