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In-vivo modulation of macrophage functions by herpes simplex virus type 2 in resistant and sensitive inbred mouse
Abstract:
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.
Insights
Herpes simplex virus type 2 (HSV-2) infection in mice influences macrophage activity and viral replication. Macrophage phagocytosis and HSV-2 replication capacity varied significantly across different mouse strains, indicating genetic influences on immune response.
Area of Science:
- Immunology
- Virology
- Genetics
Background:
- Intra-peritoneal (i.p.) infection with herpes simplex virus type 2 (HSV-2) elicits peritoneal macrophage recruitment.
- Macrophages play a crucial role in the host's innate immune response to viral infections.
Purpose of the Study:
- To investigate the correlation between mouse strain resistance to HSV-2 and macrophage phagocytic activity.
- To assess the capacity of macrophages to support HSV-2 replication in different mouse strains.
- To evaluate the impact of genetic crosses on HSV-2 replication within peritoneal exudate cells (PECs).
Main Methods:
- Intra-peritoneal inoculation of mice with HSV-2.
- Assessment of macrophage phagocytosis activity 24 hours post-infection.
- Quantification of HSV-2 replication in adherent peritoneal exudate cells (PECs).
- Analysis of HSV-2 replication in F1 hybrid mice derived from resistant and susceptible parental strains.
Main Results:
- Macrophages from moderately and highly HSV-2 resistant mouse strains exhibited enhanced phagocytosis 24 hours after infection, while low resistant strains showed limited or no response.
- The ability of macrophages to support HSV-2 replication was generally low in resistant strains but high in susceptible strains and one resistant (SJL) strain.
- F1 hybrids displayed reduced virus yields in macrophages compared to susceptible parents, with one hybrid showing superior restriction of HSV-2 replication.
Conclusions:
- Mouse strain genetics significantly influence macrophage response to HSV-2 infection, affecting both phagocytic activity and viral replication.
- Genetic factors determine the susceptibility of macrophages to support HSV-2 replication.
- Hybridization can lead to altered resistance phenotypes, suggesting potential for developing strategies to control HSV-2 infection.