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Genital Inflammation Predicts HIV-1 Shedding Independent of Plasma Viral Load and Systemic Inflammation

Blish, Catherine A. MD, PhD*,†; McClelland, R. Scott MD, MPH†,‡; Richardson, Barbra A. PhD‡,§,‖; Jaoko, Walter MBChB, PhD; Mandaliya, Kishorchandra MBChB, MRCPath#; Baeten, Jared M. MD, PhD†,‡,**; Overbaugh, Julie PhD*

JAIDS Journal of Acquired Immune Deficiency Syndromes:
doi: 10.1097/QAI.0b013e31826c2edd
Brief Report: Basic and Translational Science
Abstract

Abstract: In women, genital HIV-1 RNA levels predict the risk of HIV-1 transmission independent of plasma viral load. To better understand the factors that contribute to genital HIV-1 shedding, we evaluated the relationships between genital and plasma cytokine concentrations and HIV-1 RNA levels. Vaginal, but not plasma, levels of interferon gamma-induced protein 10 (IP-10) were significantly associated with vaginal viral load, independent of plasma viral load. Thus, efforts to decrease HIV-1 transmission must take into account the role of local inflammation, which is not necessarily reflected in plasma measurements.

Author Information

*Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, WA

Departments of Medicine

Global Health, University of Washington, Seattle, WA

§Vaccine and Infectious Diseases Division, Fred Hutchinson Cancer Research Center, Seattle, WA

Biostatistics, University of Washington, Seattle, WA

Department of Medical Microbiology, University of Nairobi, Nairobi, Kenya

#Coast General Hospital, Mombasa, Kenya

**Epidemiology, University of Washington, Seattle, WA.

Correspondence to: Catherine A. Blish, MD, PhD, Division of Infectious Diseases and Geographic Medicine, Department of Medicine, Stanford Immunology, Stanford University School of Medicine, 300 Pasteur Dr, Grant Bldg, S-101D, Stanford, CA 94305-5107 (e-mail: cblish@stanford.edu).

Supported by National Institutes of Health (NIH) Grants R37-AI038518 and P01 HD064915 (to J. Overbaugh) and Grant K08 AI068424 (to C.A. Blish). C.A. Blish also received support from a University of Washington (UW) Center for AIDS Research (CFAR) New Investigator Award, and the Mombasa study site was supported in part by the UW CFAR Grant P30 AI027757.

The authors have no conflicts of interest to disclose.

Presented as an oral abstract at the 19th Conference on Retroviruses and Opportunistic infections, March 5–8, 2012, Seattle, WA.

Received May 9, 2012

Accepted July 27, 2012

© 2012 Lippincott Williams & Wilkins, Inc.