The purpose of this dissertation was to examine if distress was associated with immunity in HIV spectrum disease, when disease severity (viral load) was used as a moderator. Distress was conceptualized as a combination of depressive and anxious symptoms; immunity was measured via a number of immune variables (three CD4+ subsets, CD8+ and two CD8+ subsets, CD19+, NK cells, PHA and NKCC). The dataset was comprised of 148 HIV seropositive men and women, who were either white, black or Hispanic recruited from the Miami-Dade community. Of these participants, 89 were asymptomatic and 59 were symptomatic, based upon Centers for Disease Control criteria (CDC, 1993). A composite distress factor score was generated using the Profile of Mood States (POMS), the Impact of Events Scale (IES), the Beck Depression Inventory (BDI), and the Perceived Stress Scale (PSS). A structural equation modeling approach was used in which immune variables were used to construct three latent immune variables. These in turn were used as outcome measures and distress factor score, viral load and the interaction of the two were used as predictors. Results indicated that distress was not related to any of the latent variables. Follow-up regression analyses were done to determine if distress related to individual immune parameters. Results showed that high distress was associated with decreased T helper (memory) cells and B-cells, but only at low levels of viral load. In addition, high distress was associated with decreased PHA, but only at high levels of viral load indicating that high viral load is associated with poorer blastogenesis in HIV. Thus, distress did not impact immune parameters in general, but impacted specific populations
