In a rural Ugandan community scaling up antiretroviral therapy (ART), we sought to determine if population-based HIV RNA levels [population viral load (VL)] decreased from 2011 to 2012.
Serial cross-sectional analyses (May 2011 and May 2012) of a defined study community of 6300 persons in a district with HIV prevalence of 8%.
We measured HIV-1 RNA (VL) levels on all individuals testing positive for HIV during a 5-day high-throughput multidisease community health campaign in May 2012 that recruited two-thirds of the population. We aggregated individual-level VL results into population VL metrics including the proportion of individuals with an undetectable VL and compared these VL metrics to those we previously reported for this geographic region in 2011.
In 2012, 223 of 2179 adults were HIV-seropositive adults (10%). Overall, among 208 of 223 HIV-seropositive adults in whom VL was tested, 53% had an undetectable VL [95% confidence interval (CI): 46 to 60], up from 37% (95% CI: 30 to 45; P = 0.02) in 2011. Seven (3%) individuals had a VL of >100,000 copies/mL in 2012, down from 21 (13%) in 2011 (P = 0.0007). Mean log (VL) (geometric mean) was 3.18 log (95% CI: 3.06 to 3.29 log) in 2012, down from 3.62 log (95% CI: 3.46 to 3.78 log) in 2011 (P < 0.0001). Similar reductions in population VL were seen among men and women.
Reductions in population VL metrics and a substantial increase in the proportion of persons with an undetectable VL were observed in a rural Ugandan community from 2011 to 2012. These findings from a resource-limited setting experiencing rapid ART scale-up may reflect a population-level effectiveness of expanding ART access.
*HIV/AIDS Division, San Francisco General Hospital, University of California, San Francisco, San Francisco, CA;
†Makerere University—University of California, San Francisco Research Collaboration, Kampala, Uganda;
‡Makerere University Joint AIDS Program, Kampala, Uganda;
§Division of Biostatistics, University of California, Berkeley, Berkeley, CA;
‖Department of Health Policy and Management, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, Chapel Hill, NC;
¶Center for AIDS Prevention Studies, Department of Medicine, University of California, San Francisco, San Francisco, CA; and
#Department of Medicine, Makerere University College of Health Sciences, Kampala, Uganda.
Correspondence to: Vivek Jain, MD, MAS, HIV/AIDS Division, San Francisco General Hospital, University of California, San Francisco, Box 0874, San Francisco, CA 94143-0874 (e-mail: firstname.lastname@example.org).
Presented as an oral abstract at the XIX International AIDS Conference (AIDS 2012), July 24, 2012, Washington, DC (abstract TULBE04).
Supported by National Institutes of Health UCSF-CTSI KL2TR000143 to V.J., a Doris Duke Clinical Scientist Development Award to M.L.P., National Institute of Allergy and Infectious Diseases at the National Institutes of Health U01 AI069502 to D.V.H., and P30 AI027763 to P. Volberding, University of California, San Francisco.
The authors have no conflicts of interest to disclose.
V.J., T.L., M.R.K., and D.V.H. designed the study. T.L. performed laboratory investigations and provided critical input on their interpretation. V.J. analyzed and interpreted data with input from M.L.P., L.B.B., E.D.C., and D.V.H. V.J. authored the article with input and important revisions from D.V.H. and all authors including D.M.B., D.K., G.C., J.K., D.M.B., T.D.C., E.H.G., and G.A.
Received July 23, 2013
Accepted September 23, 2013