Neurobiology of human herpesvirus infections.

Abstract

Critical to the adaptation of herpes simplex virus type 1 (HSV-1) to its human host is a complex interaction with the peripheral nervous system. The "life cycle" of the virus depends not only on axoplasmic transport which carries virus to and from the infected ganglia, but also on variable expression of the virus within ganglionic neurons. During latency, limited viral gene expression allows the virus to persist undetected by immune defenses, while intermittent reactivation, perhaps triggered by metabolic perturbation of these neurons, leads to production of new virus with subsequent transmission. In parasitizing its host, the virus exploits a number of the specialized properties of neurons and supporting cells. A second important type of HSV-1 infection involves the central nervous system (CNS). Herpes encephalitis, an uncommon yet severe disease, represents an aberrant interaction of the virus and host that is at present poorly understood. This review examines current understanding of HSV-1 infections of both the peripheral and CNS from a neurobiological perspective.