Leukocyte recruitment to sites of inflammation is crucial for initiating immune-mediated control of a viral infection. An inhibition of leukocyte trafficking may impair the ability of the immune system to control viral replication, thus leading to an increase in the pathology associated with viral replication. Restraint stress has been shown to alter the pattern of leukocyte recruitment and retention. For example, during a primary intranasal HSV infection, restraint stress delays both CD4+ and CD8+ T-cell recruitment into the brain of mice with symptoms of HSV encephalitis (Anglen et al., 2003). In a corneal infection model, hyperthermic stress was found to reduce the numbers of NK cells in the trigeminal ganglia of mice that were latently infected with HSV-1 (Noisakran et al., 1998). Restraint stress was found to suppress lymphadenopathy in HSV-1 infected mice. This suppression was glucocorticoid dependent as receptor blockade with the glucocor-ticoid receptor antagonist RU486 restored lymph node cellularity (Sheridan et al., 1998). In contrast, studies by Dhabhar and colleagues (Dhabhar and
McEwen, 1997, 1999) have demonstrated that an acute restraint stress session (2h) can actually enhance a lymphocyte trafficking-dependent delayed-type hypersensitivity (DTH) response in an adrenal-dependent manner. However, such a stress-induced enhancement of cell trafficking has yet to be demonstrated when using an HSV model. Alterations in leukocyte trafficking induced by psychological stress may have a profound impact on controlling viral replication and disease pathogenesis by altering the available pool of responding cells (e.g. CD8+ T cells), leading to prolonged viral replication and increased morbidity and mortality. Additional studies are needed to support this hypothesis.
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