Association Between Paired Plasma and Cervicovaginal Lavage Fluid HIV-1 RNA Levels During 36 Months

Cu-Uvin, Susan MD*; Snyder, Brad MS†; Harwell, Joseph I. MD*; Hogan, Joseph PhD†; Chibwesha, Carla MD‡; Hanley, Dawn RN*; Ingersoll, Jessica MS§; Kurpewski, Jaclynn BS*; Mayer, Kenneth H. MD*; Caliendo, Angela M. MD, PhD§

JAIDS Journal of Acquired Immune Deficiency Syndromes:
doi: 10.1097/01.qai.0000229997.52246.95
Clinical Science: Brief Report
Abstract

Objective: To determine the patterns and predictors of genital tract HIV-1 RNA levels during a 36-month period.

Methods: HIV-1 RNA levels were measured blood in plasma and the genital tract (by cervicovaginal lavage [CVL]) at baseline before highly, active antiretroviral therapy, at 2 and 4 weeks and every 6 months. Viral loads were measured using nucleic acid sequence-based amplification assay with a lower limit of detection of 2.6 log10 copies/mL.

Results: Ninety-seven women had a median of 30.4 months' follow-up, with 530 paired PVL and CVL specimens. The strongest predictor of CVL fluid HIV-1 RNA detection was PVL of more than 2.6 log10 copies/mL, with an odds ratio of 13.7 (P < 0.0001). Each log10 unit increase in PVL increased the odds of detecting HIV-1 RNA in CVL fluid by 2.6 folds (P = 0.0002). Cervicovaginal lavage fluid HIV-1 RNA exceeded PVL on 5% of visits. When patients achieved undetectable levels of HIV-1 RNA in both plasma and CVL fluid, rebound of HIV-1 RNA occurred in plasma first or concurrently with CVL fluid HIV-1 RNA.

Conclusions: Plasma viral load is the strongest predictor of CVL fluid HIV-1 RNA detection. Cervicovaginal lavage fluid HIV-1 RNA levels are generally lower than PVL. Plasma viral load is more likely to rebound first or at the same time as CVL fluid viral load.

Author Information

From *The Miriam Hospital, Brown Medical School; †Center for Statistical Sciences, Brown University; and ‡Women and Infants Hospital, Brown Medical School, Providence, Rhode Island; and §Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, Georgia.

Received for publication December 28, 2005; accepted May 18, 2006.

The authors do not have a conflict of interest.

Presented in part as a poster presentation at 11th Conference on Retroviruses and Opportunistic Infections; 2004; San Francisco, CA (abstract no. 954).

This study was supported by the National Institutes of Health (NIH) National Institute of Allergy and Infectious Diseases (NIAID) grant RO1 AI40350 and K24 AI066884 (S.C.-U.), NIH BIRCWH Scholars Program (K12 HD043447) (J.I.H.), Lifespan/Tufts/Brown University Center for AIDS Research NIH P30AI42853 (S.C.-U.), Emory Center for AIDS Research NIHAI50409 (A.M.C.), and in part by ACTG UOIAI146381 (S.C.-U.).

Reprints: Susan Cu-Uvin, MD, The Miriam Hospital, 164 Summit Avenue, Providence, RI 02906 (e-mail: scu-uvin@lifespan.org).

© 2006 Lippincott Williams & Wilkins, Inc.