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Mice previously latently infected with the F strain of herpes simplex virus type 1 (HSV-1) can be successfully colonized with a second virus strain if HSV-2 is 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 months or 3 years 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 an 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.

Retrieval of Latent Herpes Simplex Virus Type 1 Genetic Information from Murine Trigeminal Ganglia by Superinfection with Heterotypic Virus in vivo