Immunological memory is a key component of the overall immune response and is important in reducing the severity of recurrent HSV infection. Because recovery from recurrent HSV infections is largely controlled by T lymphocytes, the ability to generate a population of HSV-specific CTLm during the initial infection with HSV is thought to be critical for the long-term defense against recurrent HSV infection.The psychological stress that is often associated with the primary episode of infection, as well as the development of recurrent disease, emphasizes the potential significance of the effect of stress on the development of HSV-specific T cell-mediated immunity.
In studies to date, restraint stress has been shown not to suppress the generation of CTLm in response to systemic HSV infection. However, such a stressor has been shown to be effective at inhibiting the activation of CTLm (Bonneau et al., 1991b, 1996; Leo et al., 1998) and their migration to the site of recurrent HSV infection (Bonneau et al., 1991b). Further studies into the mechanisms underlying the suppression of CTLm activation revealed that stress does not the suppress the expression of the T-cell receptor, IL-2 receptor, and other accessory molecules required for T-lymphocyte activation. However, it does suppress the production of cytokines involved in HSV-specific CTLm activation, which is likely to be the mechanism underlying stress-induced suppression of CTLm activation (Bonneau et al., 1996). These studies were later extended to show that products of adrenal function associated with stress are responsible for suppression of cytokine production and the development of lytic activity, but they do not affect splenic cellularity (Bonneau et al., 1997). As in the studies of the primary immune response, adrenal-dependent mechanisms do not appear to be solely responsible for stress-induced suppression of memory responses to HSV infection.
Although much has been learned about the effects of stress on the generation and activation of mCTL, there is nothing known about the effects of stress, either acute or chronic, on the long-term maintenance of memory T cells in vivo and their ability to survey the body for sites of HSV infections.
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