Immunization with HSV-1 antigen rapidly protects against HSV-1-induced encephalitis and is IFN-γ independent

Herpes simplex virus type 1 (HSV-1) infection of mice frequently culminates in fatal encephalitis. Intraperitoneal administration of heat-inactivated HSV-1 0-5 days before infection (active immunization) protected mice from encephalitis. In addition, active immunization 2-5 days before ocular infection with HSV-1 reduced the frequency of establishment of latent HSV-I infection in the trigeminal ganglion (TG), However, intraperitoneal administration of heat-inactivated HSV-1 did not induce interferon (IFN) production in the peritoneum or serum, as determined by bioassay and ELISA, Intraperitoneal administration of heat-attenuated HSV-1 elicited IFN-gamma but not type I IFN production in the peritoneum, The production of IFN-gamma correlated with the infiltration of CD4 and CD8 cells in the peritoneum as determined by RT-PCR, In addition, there was a significant increase in interleukin (IL)-12 p40, IL-12p35, IL-6, IL-10, and IFN-gamma mRNA in peritoneal cells, as determined by RT-PCR following immunization with heat-attenuated HSV-1, which was not observed using heat-inactivated HSV-1, The results suggest that resistance to HSV-I is induced rapidly following immunization with viral antigen but that protection against encephalitis is independent of the cytokines that are generated in the peritoneum.