We evaluated three cellular and five serologic markers that are affected by infection with the human immunodeficiency virus type 1 (HIV-1) for their ability to predict the progression to clinical acquired immunodeficiency syndrome (AIDS). The cellular markers were the number of CD4+ T cells, the number of CD8+ T cells, and the ratio of CD4+ T cells to CD8+ T cells. The serologic markers were the serum levels of neopterin (a product of stimulated macrophages), beta 2-microglobulin, soluble interleukin-2 receptors, IgA, and HIV p24 antigen. We evaluated the usefulness of these measures as markers of the progression to AIDS prospectively, over four years, in a cohort of 395 HIV-seropositive homosexual men who were initially free of AIDS. CD4+ T cells (expressed as an absolute number, a percentage of lymphocytes, or a ratio of CD4+ to CD8+ T cells) were the best single predictor of the progression to AIDS, but the serum neopterin and beta 2-microglobulin levels each had nearly as much predictive power. The neopterin level appeared to be a slightly better predictor than the beta 2-microglobulin level. The levels of IgA, interleukin-2 receptors, and p24 antigen had less predictive value. A stepwise multivariate analysis indicated that the best predictors, in descending order, were CD4+ T cells (the percentage of lymphocytes or the CD4+: CD8+ ratio), the serum level of neopterin or beta 2-microglobulin, the level of IgA, that of interleukin-2 receptors, and that of p24 antigen. The last three markers had little additional predictive power beyond that of the first two. We conclude that of the eight markers studied, progression to AIDS was predicted most accurately by the level of CD4+ T cells in combination with the serum level of either neopterin or beta 2-microglobulin. At least one of these two serum markers, which reflect immune activation, should be used along with measurement of CD4+ T cells in disease-classification schemes and in the evaluation of responses to therapy.

Fatigued breast cancer survivors showed elevations in serum markers associated with proinflammatory cytokine activity an average of 5 years after diagnosis. Results suggest mechanisms through which enduring immune activation may occur, including alterations in cortisol and in lymphocyte subsets.

Threat to the social self is an important elicitor of shame experience, decreases in social self-esteem and cortisol increases under demanding performance conditions. Cortisol changes may be specifically tied to the experience of emotions and cognitions reflecting low self-worth in this context.

This study investigated whether finding meaning in response to an HIV-related stressor was associated with changes in immune status and health. Forty HIV-seropositive men who had recently experienced an AIDS-related bereavement completed interviews assessing cognitive processing and rinding meaning after the loss and provided blood samples for a 2-to 3-year follow-up. AIDS-related mortality over an extended follow-up was determined from death certificates. As predicted, men who engaged in cognitive processing were more likely to find meaning from the loss. Furthermore, men who found meaning showed less rapid declines in CD4 T cell levels and lower rates of AIDS-related mortality (all ps < .05), independent of health status at baseline, health behaviors, and other potential confounds. These results suggest that positive responses to stressful events, specifically the discovery of meaning, may be linked to positive immunologic and health outcomes. The ways in which individuals respond to stressful life events may influence their immune status and, potentially, their physical health. A growing number of studies in the field of psychoneuroimmunology have found that exposure to stressful experiences is associated with changes in the human immune system (for review, see Cohen & Herbert, 1996; Kemeny, Solomon, Morley, & Herbert, 1992). It has been hypothesized that these immune changes are related to cognitive and emotional responses elicited by the stressor (e.g., Cohen & Herbert, 1996). However, studies have generally failed to assess the associations between particular ways of responding to a stressor, both positive and negative, and immune outcomes. In addition, few studies have examined the health consequences of immune changes associated with stressful experiences and the psychological responses they provoke.