The possible impact of coinfection with the Kaposi sarcoma–associated herpes virus (KSHV) on the response to antiretroviral therapy (ART) is unknown. Prospective studies are rare, particularly in Africa.
We enrolled a prospective cohort of HIV-infected adults initiating ART in Johannesburg, South Africa. The subjects were defined as seropositive to KSHV if they were reactive to either KSHV lytic K8.1 or latent Orf73 antigen or to both. The subjects were followed from ART initiation until 18 months of treatment. HIV viral load and CD4 counts were tested 6 monthly. Linear generalized estimating and log-binomial regression models were used to estimate the effect of KSHV infection on immunologic recovery and response and HIV viral load suppression within 18 months after ART initiation.
Three hundred eighty-five subjects initiating ART from November 2008 to March 2009 were considered to be eligible including 184 (48%) KSHV+. The KSHV+ group was similar to the KSHV− in terms of age, gender, initiating CD4 count, body mass index, tuberculosis, and hemoglobin levels. The KSHV+ group gained a similar number of cells at 6 [difference of 10 cells per cubic millimeter, 95% confidence interval (CI): −11 to 31], 12 (3 cells per cubic millimeter, 95% CI: −19 to 25), and 18 months (24 cells per cubic millimeter, 95% CI: −13 to 61) compared with that gained by the KSHV− group. Adjusted relative risk of failure to suppress viral load to <400 copies per milliliter (1.03; 95% CI: 0.90 to 1.17) were similar for KSHV+ and KSHV− by 6 months on treatment.
In a population with a high KSHV prevalence, HIV-positive adults coinfected with KSHV achieved similar immunologic and virologic responses to ART early after treatment initiation compared with those with KSHV−.
*Health Economics and Epidemiology Research Office, Department of Internal Medicine, School of Clinical Medicine, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa;
†Clinical HIV Research Unit, Department of Internal Medicine, School of Clinical Medicine, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa;
‡Viral Oncology Section, AIDS and Cancer Virus Program, SAIC-Frederick, Frederick National Laboratory for Cancer Research, Frederick MD;
§Institute of Social and Preventive Medicine (ISPM), University of Bern, Bern, Switzerland;
‖Center for Global Health and Development, Boston, MA; and
¶Department of Epidemiology, Boston University School of Public Health, Boston, MA.
Correspondence to: Dr. Mhairi Maskew, MBBCh, MSc (Med), Health Economics and Epidemiology Research Office, Themba Lethu Clinic, Helen Joseph Hospital, Perth Road, Westdene, Johannesburg 2192, South Africa (e-mail: email@example.com).
Supported by the National Institute of Allergy and Infectious Diseases (NIAID), Grant 5U01-AI069924-05 to the International epidemiological Databases to Evaluate AIDS in Southern Africa (IeDEA-SA). This study was also made possible by the generous support of the American people through Cooperative Agreement AID 674-A-12-00,029 from the United States Agency for International Development (USAID). M.M., M.F., M.E., and D.W. also receive funding from the NIH.
The authors have no conflicts of interest to disclose.
M.M. designed the study, collected data, performed the statistical analysis, and drafted the article. P.M. assisted with study design, data collection, critical review, and editing of the article. D.W. assisted with data collection, laboratory methodology, critical review, and editing of the article. M.E. assisted with statistical analysis, critical review, and editing of the article. M.F. was involved with study design, statistical analysis, critical review, and editing of the article.
The contents are the responsibility of the authors and do not necessarily reflect the views of the USAID or of the United States Government.
Received January 04, 2013
Accepted April 09, 2013