The effect of latency-associated transcript on the herpes simplex virus type 1 latency-reactivation phenotype is mouse strain-dependent.

Abstract

Herpes simplex virus type 1 (HSV-1) latency-associated transcript (LAT) null mutants reactivate poorly in the rabbit ocular model. The situation in mice is less clear. Reports concluding that LAT null mutants reactivate poorly in the mouse explant-induced reactivation (EIR) model are contradicted by a similar number of reports of normal EIR of LAT(-) mutants in mice. To determine if the EIR phenotype might be mouse strain-dependent we infected BALB/c and Swiss Webster mice with LAT(-) or LAT(+) virus and assessed EIR in individual trigeminal ganglia. Compared to LAT(+) virus, LAT(-) virus reactivated poorly in Swiss Webster mice (P<0.05). In contrast, the EIR phenotype of these viruses was similar in BALB/c mice (P>0.1). Thus, LAT appeared to have a much greater impact on the EIR phenotype in Swiss Webster mice than in BALB/c mice. The mouse strain therefore appeared consequential in the HSV-1 EIR phenotype in mice.