Cell-mediated immunity and immunosuppression in herpes simplex virus infection.

Innate and adaptive forms of cellular immunity have important, interactive roles in host resistance to herpes simplex virus (HSV) infection. Hence, suppression of non-HSV specific and anti-HSV specific cellular immune responses can predispose the host to severe HSV infection. Studies using depletion and adoptive transfer of selected subpopulations of NK cells, macrophages, and CD4+ and CD8+ T lymphocytes indicate that each of these is of significance in protection against infection with HSV. Further evidence suggests that cytokines such as interferons alpha and gamma, interleukin 2 and leukocyte migration inhibition factor also have central roles in these cell functions during HSV infection. Of importance is that HSV itself can result in transient suppression of several innate and adaptive cellular immune responses during acute episodes of infection in normal adults. Mechanisms by which HSV may mediate this immune dysfunction include enhanced activity of suppressor T cells and soluble suppressor factors, decreases in cytokine production, decreases in expression of major and minor histocompatibility antigens and direct inhibition of cytotoxic effector cell function. Knowledge of anti-HSV cellular immunity and of the immunosuppressive properties of HSV are of importance in the development of appropriate treatment and vaccine strategies for this herpesvirus.