Abstract # 4215 Event # 93:

Scheduled for Friday, June 22, 2012 11:15 AM-11:30 AM: Session 12 (Magnolia) Oral Presentation


EFFECTS OF SOCIAL CONDITION ON NEUROENDOCRINE AND IMMUNE FUNCTION IN EARLY AND LATE SIV INFECTION IN RHESUS MACAQUES (MACACA MULATTA)

M. R. Jarcho1, K. Abel2 and J. P. Capitanio3
1University of California, Los Angeles, Cousins Center for Psychoneuroimmunology, Los Angeles, CA 90095, USA, 2University of North Carolina Medical School, Chapel Hill, NC, 27599, 3California National Primate Research Center, Davis, CA, 95616
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     Simian immunodeficiency virus impairs proper immune system functioning. Various emotional and environmental factors, including qualities of social interactions, have been shown to affect changes in immune function. This study investigated the neuroendocrine and immune responses to changes in social stability at early (n=12) and late (n=12) stages of viral infection. During stable conditions monkeys interacted with the same conspecifics each day, whereas unstable conditions involved interacting with new combinations of conspecifics for nearly every encounter. General linear models revealed that under unstable social conditions monkeys had elevated expression levels of several pro-inflammatory cytokine genes, specifically IFN-gamma, IL-6, IL-1beta, and TNF-alpha, suggesting altered immune regulation during a socially stressful time (all genes: F2>3.8, p<0.035). Importantly, cytokine expression declined when animals returned to stable social conditions. However, elevated cytokine expression was seen predominantly in animals at the early phase of viral infection, suggesting that late stage infection may be accompanied by an inability to mount an inflammatory response despite the presence of a stressor that might otherwise induce such a response. Further, plasma cortisol, but not urinary metabolites of epinephrine or norepinephrine, was higher when animals experienced social instability than when they experienced stable social conditions. These results suggest that social instability can lead to elevations in markers of inflammation, and this appears to be associated with changes in HPA axis, and not sympathetic nervous system, activity.