HSV is a natural pathogen of humans and, as noted above, is characterized by the ability to cause an acute infection at a peripheral site and to establish a latent infection in the local sensory ganglia that innervate the site of the initial infection (Blyth and Hill, 1984).The hallmark of HSV is its ability to spontaneously reactivate from this quiescent, noninfectious latent state and cause a recurrent infection in the periphery, at, or near, the site of the original infection (Hill, 1985). In humans, HSV reactivation and recurrent infections typically occur spontaneously. However, correlations have been made between reactivation and physical or emotional stress, fever, exposure to ultraviolet light, tissue damage, and immune suppression (Stevens, 1975; Hill, 1985). More recent efforts by us and others have focused on the use of mouse models to decipher the roles of psychological stress and its associated neuroendocrine components in the development of both primary and recurrent HSV infection. These models have provided a foundation for understanding the effects of stress on HSV infection.

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