Abstract
Mice previously latently infected with the F strain of herpes simplex virus type 1 (HSV-1) can be successfully colonized with a 2nd virus strain if HSV-2 introduced at the same peripheral site as HSV-1. On the other hand, HSV-1 strains seemed able mutually to exclude establishment of latency with each other. Mice (3 mo. or 3 yr after nasal infection) latently infected with HSV-1 were thus superinfected with HSV-2. The mice were sacrificed 2 days post-infection when HSV-2 replication in the ganglia was found to have commenced. Ganglia were homogenized immediately and virus was plaqued on permissive cells. HSV-1 plaques were regularly obtained among HSV-2 plaques as assessed by staining with enzyme-linked immunosorbent using a type-specific monoclonal antibody recognizing glycoprotein C of HSV-1. DNA from this virus had identical restriction endonuclease patterns (EcoRI, BamHI and HindIII) to the F strain used to infect the animals latently. HSV-1 was not retrieved from ganglia of controls superinfected with a neuroadapted vaccinia virus or were mock-superinfected. The results suggest that it is possible to superinfect a latently infected ganglionic neuronal cell with a heterotypic HSV strain and that the subsequently introduced HSV-2 can act in trans to induce reactivation of latent HSV-1.