Resistance to herpes simplex virus - type 1 (HSV-1).

Abstract

In man herpes simplex virus-type 1 (HSV-1) has been shown to be the cause of several clinically important infections, including primary gingivostomatitis, herpes keratitis, and encephalitis (Nahmias and Roizman 1973; Rawls 1973). Clinically apparent as well as inapparent infections with HSV-1 have the capacity to become latent, i.e., the virus remains dormant in neurons but can become reactivated and cause an infection at a later date (Stevens 1975). Although the mechanism(s) involved in the establishment and maintenance of latency or in the subsequent reactivation of HSV-1 are not well understood, immunosuppression does not appear to be the trigger responsible for inducing the virus to reappear (Spencer and Andersen 1970; Price and Schmitz 1978). However, HSV-1 infections have been found to be especially problematic for those afflicted with congenital or acquired immunodeficiency disorders (St. Geme et al. 1965; Aston et al. 1972; Lopez and Simmons 1977). Thus, although the incidence of reactivated HSV-1 infections is not increased with immunosuppression, clearly the severity of reactivated infections is markedly exaggerated. These observations in man as well as a number of earlier animal studies (for example, Nahmias et al. 1969) have been taken as evidence that the immune response and especially the cell-mediated immune (CMI) system plays a primary role in resistance to these infections. Because of the complex nature of the pathogenesis of HSV-1 infections, resistance probably depends on several interacting subpopulations of cells (Allison 1914). The definition of these cells, their interactions, and their relative contributions will be important to future studies aimed at augmenting resistance to HSV-1.