Abstract # 2078 Event # 128:

Scheduled for Friday, August 18, 2006 03:40 PM-04:00 PM: Session 13 (Regency East #1) Oral Presentation

Polymorphism in the serotonin transporter promoter and infectious disease

J. P. Capitanio1,2, W. A. Mason2, S. P. Mendoza2, K. Abel2 and S. A. Blozis1
1Univ. of California, Dept. of Psychology, One Shields Ave., Davis, CA 95616, USA, 2California National Primate Research Center
     Variation in the serotonin transporter gene promoter (rh5-HTTLPR) has been associated with individual differences in behavioral functioning in human and nonhuman primates. For example, others have found that possession of a short allele (which confers reduced transcriptional efficiency of the rh5-HTT gene) is associated with increased aggressiveness and altered hypothalamic-pituitary-adrenal (HPA) activity among animals experiencing adverse rearing conditions. Given the roles of hostility and HPA functioning in health and disease, these results suggest this candidate gene may affect an infectious disease process. We examined the role of rh5-HTTLPR in 24 adult male rhesus monkeys that were infected with the simian immunodeficiency virus, and that experienced daily socialization in either stable or unstable configurations. Regression analyses revealed that, overall, long/short heterozygotes showed significantly longer survival (p<.05). Early in disease, however, markers of faster progression were associated with display of aggressive behavior, which was related to genotype only for animals in the Unstable social conditions – that is, among animals in the Unstable condition (but not among animals in the Stable condition), heterozygotes were significantly (p=.045) more likely to display aggression compared to homozygous-long individuals. These data suggest that genotype can moderate animals' responses to social conditions in ways that can affect a disease process. The data also suggest differing effects of genotype depending on time-frame – early in disease versus across the entire disease course.