Format

Send to

Choose Destination
See comment in PubMed Commons below
Psychosom Med. 2008 Jun;70(5):562-8. doi: 10.1097/PSY.0b013e3181773bbd.

Psychosocial influences on HIV-1 disease progression: neural, endocrine, and virologic mechanisms.

Author information

1
Department of Medicine, Division of Hematology-Oncology, UCLA School of Medicine, the Norman Cousins Center, Jonsson Comprehensive Cancer Center, UCLA AIDS Institute, California 90095-1678, USA. coles@ucla.edu

Abstract

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.

PMID:
18541906
DOI:
10.1097/PSY.0b013e3181773bbd
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Lippincott Williams & Wilkins
    Loading ...
    Support Center