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Effects of genetic resistance against Herpes simplex virus in vaginally infected mice
Abstract:
In order to take the conditions of natural Herpes simplex virus (HSV) infection into consideration, the genetic resistance of C57-Bl mice, which was established by intraperitoneal HSV-1 infection [Lopez, 1975], was investigated in vaginally infected mice. The course of infection in the mucous membranes did not differ in sensitive (NMRI) and resistant (C57-Bl) mice: both number of takes and virus elimination from the vagina were equal, and no difference in viral titer produced in the vagina was detected. Viral titer in the productively infected lumbosacral ganglia, however, was less in the resistant mice. An experiment with foot-pad-infected mice confirmed that the number of productively infected ganglia was reduced in resistant mice, and contralateral ganglia were infected only in the sensitive mouse strain. In spite of this, the number of latently infected animals did not vary significantly in the mouse strains. Higher activity of defense mechanisms in resistant mice, apparently localized in the ganglia, resulted in reduced lethality. As to the mechanisms of the resistance, neither antibody nor interferon response were enhanced in C57-Bl mice, but resistance was abolished by depletion of several cellular functions, i.e., lymphocytes by cyclophosphamide or X-rays, macrophages by silica or macrophage-antiserum, and M-cells by 89Sr.
Insights
Genetic resistance in C57-Bl mice to Herpes simplex virus (HSV) infection was studied. Resistant mice showed reduced viral load in ganglia and lower lethality, despite similar vaginal infection levels compared to sensitive mice.
Area of Science:
- Immunology
- Virology
- Genetics
Background:
- Herpes simplex virus (HSV) infection models often use intraperitoneal inoculation.
- Understanding HSV pathogenesis in natural infection routes, like vaginal exposure, is crucial.
- Genetic resistance to HSV varies among mouse strains, impacting disease outcomes.
Purpose of the Study:
- To investigate the genetic resistance of C57-Bl mice to vaginal HSV-1 infection.
- To compare HSV infection course and viral titers in resistant (C57-Bl) and sensitive (NMRI) mice.
- To explore the cellular mechanisms underlying HSV resistance in C57-Bl mice.
Main Methods:
- Vaginal and foot-pad inoculation of HSV-1 in C57-Bl and NMRI mice.
- Assessment of vaginal infection, virus elimination, and viral titers in ganglia.
- Depletion of cellular components (lymphocytes, macrophages, M-cells) to assess resistance mechanisms.
Main Results:
- No difference in vaginal infection take or virus elimination between resistant and sensitive mice.
- Resistant mice exhibited lower viral titers in productively infected lumbosacral ganglia and reduced contralateral ganglia infection.
- Cellular depletions (lymphocytes, macrophages, M-cells) abolished resistance, indicating their crucial role.
Conclusions:
- C57-Bl mice display genetic resistance to HSV infection, primarily impacting ganglia involvement and reducing lethality.
- Resistance is mediated by cellular defense mechanisms localized in the ganglia, not by antibody or interferon responses.
- Lymphocytes, macrophages, and M-cells are critical for mediating HSV resistance in C57-Bl mice.