To define the effect of heterogeneity of murine peritoneal macrophages (Mø) on intrinsic resistance to herpes simplex virus (HSV) infection, several Mø populations were characterized for their response to infection with HSV type 1 (HSV-1) and HSV-2. Steady-state resident Mø (Res Mø) were compared in parallel with Mø activated with (now designated ) (CP Mø) and thioglycollate-elicited inflammatory Mø (TG Mø). Res Mø were completely non-permissive for productive virus infection and showed no c.p.e. The intrinsic resistance of CP Mø to HSV infection was similar to that of Res Mø, in that the infection was non-productive for infectious virus, but CP Mø showed marked c.p.e. TG Mø showed semi-permissiveness, with virus yields at least 10-fold higher than those in Res Mø and CP Mø, and marked c.p.e. The three distinct intrinsic response patterns were maintained regardless of whether Mø were derived from CD-1 or B6C3F1 mice, or whether the infecting virus was HSV-1 or HSV-2. To define the level at which Mø restrict HSV replication, immunofluorescence assays for viral antigens and hybridization analyses for viral DNA were performed. All Mø populations showed immediate early and early virus polypeptides. Res Mø and CP Mø showed no viral DNA replication, but TG Mø showed moderate levels of viral DNA synthesis that paralleled the infectious virus titres produced. Investigation of the mechanism for the heterogeneous intrinsic antiviral response among the Mø revealed that interferon was not involved, because antiserum to mouse α/β interferon did not alter the intrinsic resistance patterns. Induction of c.p.e. in Mø required live, replication-competent HSV. The involvement of tumour necrosis factor (TNF) in c.p.e. was found to be unlikely; no significant amounts of TNF were detected in the culture medium of the Mø, and inclusion of anti-TNF antibody did not inhibit c.p.e.

Keyword(s): HSV , macrophages and resistance

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