ABSTRACT
This chapter reviews some aspects of the pathogenesis of Herpes simplex virus (HSV)-1 and HSV-2 infections, with emphasis on data derived from humans as hosts and from their viral isolates. An important limitation in the field of HSV pathogenesis is the difficulty in studying asymptomatic infection, which therefore remains enigmatic. HSV envelope glycoproteins play a major role during viral entry and egress, and are dominant targets for human B- and T-cell mediated immune responses as well as mediators of immune evasion such as binding of complement factors and the Fc part of Immunoglobulin G. HSV entry is a cascade reaction initiated by interaction of glycoprotein C with cell surface glycosaminoglycans such as heparan sulfate and chondroitin sulfate. The biological property of reactivation is central to the medical scope of HSV infection. Common triggering events of HSV induced peripheral lesions caused by viral reactivation include nerve trauma, septicaemia and other infections, Ultraviolet-irradiation, dental procedures, and possibly also persistent mental stress.
