The Impact of Stress on Primary HSV Infection

The ability to limit the amount of HSV replication during a primary infection may, in turn, reduce the amount of latent virus that colonizes the local sensory ganglia (Bonneau and Jennings, 1989). Therefore, by destroying HSV-infected cells before progeny virions can be produced may actually limit the extent of neuronal involvement and reduce the amount of latent virus within these ganglia. Therefore, the impact of a stressor on the immune response during the primary HSV infection may have consequences on not only one's initial encounter with HSV but also on the development of recurrent HSV infections throughout the lifetime of the host.

Studies in humans have indicated that stress can affect the frequency, severity, and duration of HSV infection. A number of murine studies during the past 15 years have substantiated these findings by providing compelling experimental evidence that stress and stress-induced, neuroendocrine-derived products increase the development and severity of HSV infection in both the periphery (Bonneau et al., 1991a; Kusnecov et al., 1992; Bonneau et al., 1997; Brenner and Moynihan, 1997; Wonnacott and Bonneau, 2002) and the central nervous system (Anglen et al., 2003). For example, mouse models in which either a restraint (Bonneau et al., 1991a; Wonnacott and Bonneau, 2002; Ortiz et al., 2003) or footshock (Kusnecov et al., 1992) model of stress were used were shown to result in increased HSV titers at a site of local, HSV infection. Stress was also shown to suppress the ability of adoptively transferred lymphocytes with HSV-specific lytic activity to confer protection against lethal HSV infection in an immunocompromised host as well as inhibiting the restoration of immune responsiveness to HSV infection after sublethal gamma irradiation (Bonneau et al., 1997). These latter findings are important because adoptive immunotherapy represents a potentially effective approach by which to control the extent of viral infections in an immunocompromised host. Other studies using the glucocorticoid antagonist androstenediol (AED) have shown that AED can significantly improve the survival of mice with HSV-1-induced encephalitis. Moreover, it was shown that this increased level of protection was mediated by an augmentation in type I interferon production (Daigle and Carr, 1998). As noted above, recent studies from our laboratory have focused on the impact of maternal stress on the transfer of antibody from mother to fetus/neonate. In these studies, we have demonstrated that increased levels of postpartum maternal corticosterone increases neonatal susceptibility to HSV-2-associated infection by reducing the amount of HSV-specific antibody transferred via the transmammary route (Yorty et al., 2004b).

As was described earlier, these studies have shown that stress suppresses components of the primary CTL responses to HSV infection (Bonneau et al, 1991a; Kusnecov et al., 1992; Bonneau et al, 1993; Dobbs et al, 1993; Bonneau, 1997; Brenner and Moynihan, 1997; Leo et al., 1998; Leo and Bonneau, 2000a,b) and memory (Bonneau et al., 1991b; Bonneau, 1996, 1998; Leo et al., 1998; Leo and Bonneau, 2000a; Wonnacott and Bonneau, 2002). By using a combination of surgical and pharmacological approaches, a role for both the HPA axis (Bonneau et al., 1993,1998) and the sympathetic nervous system (Leo and Bonneau, 2000a,b) has clearly been demonstrated as one of the underlying mechanisms mediating stress-induced modulation of immunity and HSV-associated pathology.

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