Effects of genetic resistance against Herpes simplex virus in vaginally infected mice.

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.