A mutant deleted for most of the herpes simplex virus type 1 (HSV-1) UOL gene does not affect the spontaneous reactivation phenotype in rabbits

The mechanisms involved in the herpes simplex virus type 1 (HSV-1) latency-reactivation cycle are not fully understood. The latency-associated transcript (LAT) is the only HSV-1 RNA abundantly detected during neuronal latency. LAT plays a significant role in latency because LAT(-) mutants have a reduced reactivation phenotype. Several novel viral transcripts have been identified within the LAT locus, including UOL, which is located just upstream of LAT. The authors report here on a mutant, ΔUOL, which has a 437-nucleotide deletion that deletes most of UOL. ΔUOL replicated similarly to its wild-type parental McKrae HSV-1 strain in infected cells, the eyes, trigeminal ganglia, and brains of mice and rabbits. It was indistinguishable from wild-type virus as regards explant-induced reactivation in mice, and spontaneous reactivation in rabbits. In contrast, ΔUOL was significantly less virulent in mice. Thus, UOL appears to be dispensable for the wild-type reactivation phenotype while appearing to play a role in neurovirulence in ocularly infected animals.