Herpes simplex virus type 2 establishes latency in the mouse footpad and in the sensory ganglia.

Three mouse strains as well as wt and 7 ts mutants of herpes simplex virus (HSV) type 2 (strain HG52) have been used to investigate latency. The mice were inoculated in the right rear footpad. Virus reactivation following explanation and culture of the dorsal root ganglia and the footpad was scored. The results show that: HSV-2 can be maintained in the mouse footpad in a state indistinguishable from latency; virus gene functions necessary for latency can be identified by the use of ts mutants; and mouse strains differ in their ability to support latent infection. An infectious center assay was used to quantitate virus reactivation from dissociated dorsal root ganglia. HSV-1 strain 17 wt spread after inoculation at doses of greater than or equal to 5.0 X 10(5) plaque-forming units (pfu), producing latency also in contralateral ganglia but with lower efficiency.