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BIOBEHAVIORAL MECHANISMS |
From the Department of Medicine, Division of Hematology-Oncology, UCLA School of Medicine, the Norman Cousins Center, Jonsson Comprehensive Cancer Center, UCLA AIDS Institute, and UCLA Molecular Biology Institute, Los Angeles California.
Address correspondence and reprint requests to Steve W. Cole, PhD, 11-934 Factor Building, UCLA School of Medicine, Los Angeles, CA 90095-1678. E-mail:coles{at}ucla.edu
This review surveys empirical research pertinent to the hypothesis that activity of the hypothalamus-pituitary-adrenal (HPA) axis and/or the sympathetic nervous system (SNS) might mediate biobehavioral influences on HIV-1 pathogenesis and disease progression. Data are considered based on causal effects of neuroeffector molecules on HIV-1 replication, prospective relationships between neural/endocrine parameters and HIV-relevant biological or clinical markers, and correlational data consistent with in vivo neural/endocrine mediation in human or animal studies. Results show that HPA and SNS effector molecules can enhance HIV-1 replication in cellular models via effects on viral infectivity, viral gene expression, and the innate immune response to infection. Animal models and human clinical studies both provide evidence consistent with SNS regulation of viral replication, but data on HPA mediation are less clear. Regulation of leukocyte biology by neuroeffector molecules provides a plausible biological mechanism by which psychosocial factors might influence HIV-1 pathogenesis, even in the era of effective antiretroviral therapy. As such, neural and endocrine parameters might provide useful biomarkers for gauging the promise of behavioral interventions and suggest novel adjunctive strategies for controlling HIV-1 disease progression.
Key Words: HIV-1 • disease progression • sympathetic nervous system • HPA axis • neuroendocrine • catecholamine • norepinephrine • cortisol
Abbreviations: HPA = hypothalamus-pituitary-adrenal; SNS = sympathetic nervous system; NE = norepinephrine;SIV = Simian Immunodeficiency Virus; ART = antiretroviral therapy; CTL = cytotoxic T lymphocyte.
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