Marsland, S. Cohen, Rabin, and Manuck (in press) further explored whether individual differences in immune reactivity are germane to susceptibility to infectious disease. This study examined whether immune reactivity predicted antibody response to recombinant hepatitis B vaccination, an in vivo measure of host resistance to viral infection. For this purpose, 84 healthy graduate students who tested negative for prior exposure to hepatitis B virus were administered the standard series of three hepatitis B vaccinations. The first two vaccinations were given 6 weeks apart, with a follow-up booster dose administered 6 months following the first shot. Five months after the first dose, each subject completed a battery of stress measures and a blood sample was drawn to assess hepatitis B surface antibody levels. Four to 6 weeks following completion of the vaccination series, subjects returned to the laboratory to perform an acute laboratory stress protocol, measuring immunologic responses to an evaluative speech task. Findings demonstrated that, when compared with high antibody responders, subjects who mounted lower antibody responses to hepatitis B vaccination following the first two doses displayed greater stress-induced suppression of immune function, as measured by proliferative response to PHA, but not Con A or PWM. As such, this study lends some support to the hypothesis that individual differences in the magnitude of stress-induced suppression of immune function may have clinical significance, being related to an in vivo immune response relevant for protection against infection. Consistent with other studies measuring the impact of stress later in the antibody response (Jabaaij et al., 1993; Snyder et al., 1993; Stone et al., 1994), no association was found between stress and antibody response.
At present, the clinical significance of the observed differences in magnitude of antibody response among the high and low responders is unknown. This study was conducted using young, healthy participants and a vaccination protocol designed to produce maximal immunity to hepatitis B in greater than 90% of individuals. Hence, the majority of subjects show an antibody titer that is considered to be protective against hepatitis B infection by the end of the vaccination series. However, it is known that individuals who mount lower antibody responses to hepatitis B vaccination lose their protective status more quickly (Horowitz, Ershler, McKinney, & Battiola, 1988). Hence, subjects who showed greater immune reactivity following acute stress might be expected to have a decreased duration of immunity to hepatitis B than individuals who are less immunoreactive. It is also possible that individual differences in reactivity would have a greater impact on vaccination response among less healthy populations (e.g., elderly or very young persons) or those who already have compromised immune function (e.g., individuals with HIV or cancer).
In sum, some initial evidence is provided that individual differences in the magnitude of immune responses to acute laboratory challenge are related to an in vivo measure of immune competence. However, prospective studies employing measures of individual difference as predictors of disease outcome are required in order to show that individuals who show greater suppression of immune function following stress are more vulnerable to infectious disease.
In support of popular belief, there is now substantial evidence for the role of psychological stress in susceptibility to upper respiratory infectious disease (e.g., S. Cohen et al., 1991; Stone et al., 1992). One possible mediator of this relation is the modulation of immune function, thereby influencing host susceptibility to infectious pathogens. In this regard, it is well established that both major stressful experiences (e.g., bereavement or natural disasters) and more minor stressors (e.g., arguing with a spouse, acute laboratory challenge) are associated with changes in immune function. However, it remains unclear whether associations between psychological factors and infectious disease are attributable to stress-induced changes in immunity. Indeed, the clinical significance of relatively small immunologic alterations has not been established. Many associations between stress and health or between stress and the immune system may be attributable to concomitant changes in health behaviors. Recent studies conducted in laboratory settings, however, provide evidence that the sympathetic nervous system mediates some immunologic changes during acute challenge stress. It has also been demonstrated that individuals differ substantially in the magnitude of their immunologic responsivity to stress, with recent evidence suggesting that these response tendencies may reflect stable attributes of individuals. Hence, it is conceivable that there is a meaningful distribution of differences in immunologic reactivity that may form a physiological basis for differences in susceptibility to infection.
Future research in psychoneuroimmunology needs to focus on whether the type or magnitude of stress-related immune modulation influences host resistance to disease, especially in light of the fact that immune responses of stressed persons generally fall within normal ranges (Rabin, S. Cohen, Ganguli, Lysle, & Cunnick, 1989). Indeed, it has been suggested that substantial fluctuations in immune function can be tolerated without producing increased susceptibility to disease (S. Cohen, 1988). The role of the immune system in susceptibility to infectious disease needs to be addressed with prospective studies, measuring psychosocial parameters and immune mediators relevant for the disease under study, controlling for health behavior, and documenting
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