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Plasma and cervical viral loads among Ugandan and Zimbabwean women during acute and early HIV-1 infection

Morrison, Charles Sa; Demers, Koreyb; Kwok, Cynthiac; Bulime, Stanleyd; Rinaldi, Annea; Munjoma, Marshalle; Dunbar, Meganf; Chipato, Tsungaie; Byamugisha, Josaphatg; Van Der Pol, Barbarah; Arts, Erici; Salata, Robert Ai

doi: 10.1097/QAD.0b013e32833433df
Epidemiology and Social

Objectives: High levels of HIV-1 viremia exist in peripheral blood during acute and early infection; however, data on HIV-1 viral loads in female genital secretions during this period are sparse.

Design: Prospective cohort of 188 African women with primary HIV-1 infection.

Methods: HIV-uninfected and infected women were followed quarterly; we tested serial plasma specimens by HIV PCR to estimate infection dates. We used the Loess procedure to estimate the magnitude and timing of viral setpoints in plasma and cervical secretions and generalized estimating equations (GEE) to identify predictors of plasma and cervical viral setpoints.

Results: We estimated the mean HIV-1 plasma setpoint to be 4.20 log10 HIV-1 RNA copies/ml [95% confidence interval (CI) 4.04–4.35] at 121 days (95% CI 91–137) from infection; an analogous mean cervical viral setpoint was 1.64 log10 HIV-1 RNA copies/swab (95% CI 1.46–1.82) at 174 days (95% CI 145–194) from infection. Cervical loads were significantly higher (0.7–1.1 log10 copies/swab) during acute infection than subsequently. Subtype D infection, pregnancy, breastfeeding, and older age at the time of infection were associated with higher plasma viral setpoint. Subtype C infection, nonviral sexually transmitted infections, having a partner spending nights away from home, recent unprotected sex, and shorter time since infection were associated with higher cervical HIV-1 loads. Hormonal contraception was not associated with either the HIV-1 plasma setpoint or cervical loads during early infection.

Conclusion: Cervical HIV-1 viral loads were highest during acute infection and then declined up to 6 months following infection, when a ‘setpoint’ was attained. The prognostic value of a cervical ‘setpoint’ on future transmission risk remains unclear.

aBehavioral and Biomedical Research Department, Family Health International, Research Triangle Park, North Carolina, USA

bCell and Molecular Biology Graduate Group, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA

cBiostatistics Department, Family Health International, Research Triangle Park, North Carolina, USA

dJoint Clinical Research Centre, Kampala, Uganda

eDepartment of Obstetrics and Gynaecology, University of Zimbabwe, Harare, Zimbabwe

fWomen's Global Health Imperative, Research Triangle Institute, San Francisco, California, USA

gFaculty of Medicine, Makerere University, Kampala, Uganda

hBehavioral Sciences Program, Indiana University School of Medicine, Indianapolis, Indiana, USA

iDepartment of Medicine, Case Western Reserve University, Cleveland, Ohio, USA.

Received 20 March, 2009

Revised 5 October, 2009

Accepted 14 October, 2009

Correspondence to Charles S. Morrison, PhD, Family Health International, PO Box 13950, Research Triangle Park, NC 27709, USA. Tel: +1 919 544 7040; fax: +1 919 544 7261; e-mail: cmorrison@fhi.org

© 2010 Lippincott Williams & Wilkins, Inc.