Abstract # 99:

Scheduled for Sunday, September 14, 2014 10:45 AM-11:00 AM: Session 15 (Henry Oliver) Oral Presentation


LOW SOCIAL RANK PRIOR TO SIV OR SHIV INFECTION ASSOCIATES WITH HIGHER VIRAL LOAD IN CHRONIC INFECTION OF INDIVIDUALLY HOUSED RHESUS MACAQUES

G. N. Neigh1,2,3,4, T. Hayes1,4, R. Trible1,4, T. H. Vanderford1,4, D. G. Carnathan1,4, K. Easley1, M. Paiardini1,4 and G. Silvestri1,4
1Emory University, 615 Michael Street, Suite 600, Atlanta, GA 30322, USA, 2Department of Physiology, 3Department of Psychiatry & Behavioral Sciences, 4Yerkes National Primate Research Center
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     The tempo of disease progression in HIV-infected humans and SIV-infected rhesus macaques (Macaca mulatta) is variable among individuals. Prolonged exposure to stress alters immune system function and shortens survival time in SIV-infected macaques. Macaques establish a matriarchal hierarchy in which subordinate animals consistently demonstrate elevated markers of chronic stress compared to dominant ones. We tested the hypothesis that stress history, as dictated by subject’s social rank prior to study assignment, predicts plasma viral load (PVL) and disease progression during chronic SIV infection. Retrospective individual animal meta-analysis was conducted on PVL and CD4 data across acute and chronic phases of infection. PVLs were measured by RTPCR as copies of SIV RNA/ml of plasma. From blood absolute CD4+ T-cell counts and Ki-67 expression were measured by flow cytometry. Sixty-two infected macaques were stratified based on the pre-infection social rank and evaluated longitudinally. In the acute phase of infection, neither virus replication nor absolute CD4+ T-cell count were predicted by social rank prior to study assignment (p>0.05). During chronic infection, social rank prior to study assignment influenced the level of virus replication and absolute CD4 count (p<0.05). These data demonstrate that social history prior to SIV/SHIV infection influences PVL and CD4 count in chronic disease, with increased exposure to stress associated with higher levels of virus replication, increased depletion of CD4+ T-cells, and increased activation of CD4+ T-cells.