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Lack of Decay of HIV-1 in Gut-Associated Lymphoid Tissue Reservoirs in Maximally Suppressed Individuals

Poles, Michael A. MD, PhD; Boscardin, W. John PhD*; Elliott, Julie MS*; Taing, Philip BS*; Fuerst, Marie M.P. MS, RN*; McGowan, Ian MD, PhD*; Brown, Stephen MD; Anton, Peter A. MD*

JAIDS Journal of Acquired Immune Deficiency Syndromes: September 2006 - Volume 43 - Issue 1 - p 65-68
doi: 10.1097/01.qai.0000230524.71717.14
Clinical Science: Brief Report

Summary: Although peripheral blood mononuclear cells (PBMCs) and lymph nodes represent a principal reservoir, the contribution of gut-associated lymphoid tissue (GALT) has not been evaluated. In 15 HIV-1-infected subjects with maximal suppression of HIV replication by highly active antiretroviral therapy, we quantified HIV-1 DNA and RNA in mucosal biopsy specimens, PBMCs, and plasma with ultrasensitive assays. We also calculated compartmental burdens of HIV-1 DNA-positive cells and characterized the temporal decay of these reservoirs in a period of 1 year (with projections to >50 years). HIV-1 RNA was detected in 20% of the subjects' mucosal biopsy specimens and in 80% of the PBMC samples. Mucosal HIV-1 DNA was detected in 80% of the subjects and in 100% of the PBMC samples. Calculated numbers of lymphoid cells containing "potentially replication-competent" HIV-1 DNA showed that the PBMC compartment contained approximately 70,000 such cells, and GALT contained approximately 160,000 cells. Rates of decay slopes for all 15 subjects in both compartments were not statistically significantly different when compared with each other or with zero slope. Our data indicate that GALT is a quantitatively important reservoir of potentially replicative cells containing HIV-1 DNA, harboring at least as many or more of such cells as the PBMC compartment. In well-suppressed patients on highly active antiretroviral therapy, the GALT compartment showed no clear pattern of HIV-1 decay, similar to that in the PBMCs.

From the *Center for Prevention Research at David Geffen School of Medicine, University of California-Los Angeles AIDS Institute, University of California-Los Angeles, Los Angeles, CA; †Aaron Diamond AIDS Research Center, New York University School of Medicine, New York, NY; and ‡AIDS Research Alliance, West Hollywood, CA.

Received for publication December 14, 2005; accepted May 18, 2006.

Drs M. A. Poles and W. J. Boscardin contributed equally to the study design, undertaking, analysis, and manuscript preparation.

This work was supported by NIH AI 01610 (P.A.A.); NIH AI 01668 (M.A.P.); the University of California-Los Angeles Center for AIDS Research (NIH AI28697) Cores of Mucosal Immunology, Virology, and Biostatistics; AIDS Research Alliance in West Hollywood; Macy's Foundation; the Pendleton Foundation; and the Oppenheimer Brothers' Foundation.

Reprints: Peter A. Anton, MD, Department of Medicine, David Geffen School of Medicine, University of California-Los Angeles AIDS Institute, University of California-Los Angeles, 675 Charles E. Young Dr South, MRL 2734, Los Angeles, CA 90095 (e-mail: panton@mednet.ucla.edu).

© 2006 Lippincott Williams & Wilkins, Inc.