Neural infection in mice after cutaneous inoculation with HSV-1 is under complex host genetic control.

The ability to restrict neural infection with herpes simplex virus is of potential importance because the nervous system is the main reservoir of virus between recrudescences. Genetic control of innate resistance to herpes simplex after intraperitoneal challenge is well established, but this route of infection does not mimic the progress of virus from skin to the sensory nervous system which occurs during natural infection. We show here, by Mendelian analysis, that the control of neural infection after cutaneous inoculation is complex, involving several (perhaps four) genetic loci, and is not accurately represented by genes which determine survival. The results are discussed in relation to possible underlying resistance mechanisms, particularly the control of early interferon production.