Abstract # 13211 Event # 33:

Scheduled for Thursday, August 9, 2018 10:15 AM-10:30 AM: (Chula Vista ) Oral Presentation


K. Metcalf Pate1, S. Guerrero-Martin1, K. McGee2 and L. Rubin1
1Johns Hopkins University School of Medicine, Dept of Molecular and Comparative Pathobiology, 733 North Broadway / MRB 847, Baltimore, MD 21205, USA, 2Notre Dame of Maryland University
     Simian immunodeficiency virus (SIV)-infected macaques are a valuable animal model for the study of HIV infection, and may be singly or socially housed depending on the research study. Singly housed uninfected macaques show signs of stress, including immunosuppression. SIV also causes immunosuppression, as reflected most prominently by the decline in CD4+ T cell counts that is commonly used to monitor disease progression. We hypothesized that socially housed SIV-infected macaques would demonstrate less immunosuppression and more control of viral replication compared with singly housed SIV-infected macaques. We compared CD4+ T cell counts and viral loads from 35 singly and 41 socially housed SIV-infected pigtailed macaques (Macaca nemestrina); all macaques were socially housed in compatible pairs or groups prior to inoculation, with singly housed macaques transitioning to single housing on inoculation day while socially housed macaques remained with their pre-inoculation partners. Singly housed macaques demonstrated more profound decline in the percentage of circulating CD4+ T cells throughout acute infection compared to socially housed macaques (P < 0.0001). Singly housed macaques furthermore had higher viral loads in plasma and cerebral spinal fluid throughout acute infection compared to socially housed macaques (P < 0.001), and greater variability in plasma viral load data (P < 0.0001). These data imply that single housing may provide an exogenous cause of immunosuppression with the potential to confound results and reproducibility in HIV research.