An HSV-1 mutant lacking the LAT TATA element reactivates normally in explant cocultivation.

In order to examine if mutations within the LAT promoter region of HSV-1 are sufficient to change the reactivation phenotype, a mutant (KOS/29) containing a deletion of the LAT TATA element was used to establish latent infections in mouse ganglia by corneal inoculation. During the acute phase of infection, KOS/29 replicated as efficiently as its wild-type parent. As previously noted, latent KOS/29 infections were totally devoid of LAT gene transcripts (Dobson A. T., Sederati F., Devi-Rao G., Flanagan J., Farrell M. J., Stevens J. G., Wagner E. K., and Feldman L. T., J. Virol. 63, 3844-3851 (1989))). However, unlike other null mutants, KOS/29 reactivated from explanted ganglia with a kinetics similar to that of the LAT competent parent. These data show that the deletion created in KOS/29, removing the LAT TATA promoter element and small upstream and downstream flanking sequences, is not enough to alter the reactivation phenotype and that efficient reactivation can occur in the absence of any detectable LAT expression during latency.