Wu L, Eisenstein T K, Morahan P S
Department of Microbiology and Immunology, Medical College of Pennsylvania, Philadelphia 19129.
Adv Exp Med Biol. 1992;312:167-72. doi: 10.1007/978-1-4615-3462-4_17.
The intrinsic resistance to herpes simplex virus type 1 (HSV-1) of murine peritoneal macrophages (PM phi) obtained after in vivo infection of different stimuli has been investigated and shown to vary depending on the state of M phi activation. Activation of M phi by C. parvum (CP-M phi) or by an avirulent strain of S. typhimurium (Sal-M phi) increased the permissiveness of M phi to HSV-1 infection as evidenced by increased HSV-1 immediate early (IE) gene expression, synthesis of IE proteins, and the degree of cytopathic effect. HSV-1 infection was also found to sharply reduce the level of IL-1-beta mRNA in CP-M phi) and Sal-M phi, and the level of IL-3 mRNA in infected Sal-M phi, as measured by northern blot hybridization. Barely detectable levels of IL-beta mRNA were found in Sal-M phi after infection with HSV-1 when the polymerase chain reaction (PCR) assay was used to confirm the reduction of IL-1-beta mRNA. These data suggest that HSV-1 infection can modulate gene expression of some cytokines in the activated M phi.