In-vivo modulation of macrophage functions by herpes simplex virus type 2 in resistant and sensitive inbred mouse strains.
Intra-peritoneal (i.p.) infection of mice with herpes simplex virus type 2 (HSV 2) attracted macrophages into the peritoneum. Macrophages from moderately and highly HSV 2 resistant mouse strains expressed elevated phagocytosis activity 24 hours after injection. Stimulation of phagocytosis in low resistant strains was generally less effective or absent. This was, in some experiments, due to the fact that macrophages were already highly activated before the experimental infection. I.p. infection also caused HSV replication in the adherent peritoneal exudate cell (PEC) population. The capacity of macrophages supporting HSV 2 replication was low in three of four resistant mouse strains and high in all moderately and highly susceptible and in one of the resistant (SJL) strains when determined 24 hours after infection. Four different F1 hybrids between resistant and susceptible strains exhibited significantly lower yields of virus-producing macrophages than the HSV-sensitive parent. One hybrid between two HSV-susceptible lines restricted virus replication in the PEC populations better than both parental strains.
D000818:Animals; D004198:Disease Susceptibility; D006561:Herpes Simplex / Q000276:immunology*; D006824:Hybridization, Genetic; D007113:Immunity, Innate; D008262:Macrophage Activation; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains / Q000276:immunology*; D010587:Phagocytosis