Given the role that the immune system plays in the resistance to many viral infections, including HSV, vaccination remains an often desired strategy by which to confer protection. However, identifying the salient immune components that are involved in this protection may represent an obstacle to the design of an effective vaccine. The complex nature of HSV infections may also provide a formidable challenge to the development of a vaccine that would be effective at all stages of infection and at multiple sites within the body. Even if a vaccine were to be developed, the fact that stress has been shown to suppress the induction of vaccine-induced immunity (Glaser et al., 1992; Kiecolt-Glaser et al, 1996; Vedhara et al, 1999; Glaser et al, 2000; Burns et al., 2002; Miller et al., 2004) suggests that not all individuals who are vaccinated may necessarily be protected. Moreover, the impact of stress on the reactivation of immunological memory may suppress vaccine-mediated protection against infection.
Despite long-term efforts, there is currently not a vaccine to prevent either a primary HSV infection or an infection arising from reactivation of HSV from the latent state. However, there are a variety of therapeutic agents that have been designed to interfere directly with viral replication (acyclovir, penciclovir), are converted in vivo to acyclovir or penciclovir (valacyclovir HCl and famciclovir, respectively), or prevent the virus from fusing to cell membranes, thus barring virus entry into the cell (docosanol). These drugs may be beneficial by reducing the severity and shortening the course of recurrent infections and may aid in lowering the incidence of future outbreaks by reducing the amount of latent virus in the neural ganglia. However, they do not prevent recurrences entirely and therefore do not eliminate the possibility of spreading an HSV infection from one individual to another. However, a reduced viral load and shorter duration of infection may reduce this possibility to some extent. The effectiveness of these drugs may be enhanced by an effectively functioning immune system. Thus, the effects of stress on immune function may be important even when drug therapy is the chosen treatment strategy.
Any effective strategy to eliminate HSV infections from the general population will need to not only prevent a primary infection but also the establishment of a latent infection. For those individuals already harboring latent HSV, the ability of this strategy to either eliminate the latent virus, inhibit its reactivation, and/or block the development of recrudescent disease after reactivation is desirable. However, it is unlikely that any one treatment strategy will be effective in accomplishing each of the above objectives in preventing HSV infection.
What role could controlling stress play in the prevention of recurrent HSV? First, despite the many facets of an HSV infection, it is clear that the immune system plays a role, to some degree, in one's ability to prevent and/or recover from infection. Second, psychological stress has been shown to be intimately linked to the development of recurrent HSV infections— most likely through the suppression of both HSV-specific and nonspecific immune defense mechanisms. As is outlined above, a number of life events, some of which are inherently stressful, have been shown to be associated with outbreaks of recurrent HSV infection. Such events may, in part, dictate why some individuals have frequent reactivation events and other individuals have few. Therefore, limiting the degree of psychological stress may, in some cases, be adequate for maintaining a sufficient immune defense against HSV infection. This limiting of stress may be accomplished though a variety of behavioral modification and social support mechanisms.
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