Abstract
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-1 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-γ but not type I IFN production in the peritoneum. The production of IFN-γ 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-γ 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-1 is induced rapidly following immunization with viral antigen but that protection against encephalitis is independent of the cytokines that are generated in the peritoneum.
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