Abstract: HIV-1 subtype D is associated with faster disease progression compared with subtype A. Immunological correlates of this difference remain undefined. We investigated invariant natural killer T (iNKT) cells and FoxP3+ regulatory T cells (Tregs) in Ugandans infected with either subtype. Loss of iNKT cells was pronounced in subtype D, whereas Tregs displayed more profound loss in subtype A infection. The iNKT cell levels were associated with CD4 T-cell interleukin-2 production in subtype A, but not in D, infection. Thus, these viral subtypes are associated with differential loss of iNKT cells and Tregs that may influence the quality of the adaptive immune response.
*Makerere University Walter Reed Project, Kampala, Uganda;
†Department of Medicine, Center for Infectious Medicine, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden;
‡US Military HIV Research Program, Silver Spring, MD;
§Division of Intramural research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD;
‖Johns Hopkins School of Medicine, Baltimore, MD;
¶School of Public Health, Makerere University College of Health Sciences, Kampala, Uganda;
#Rakai Health Sciences Program, Uganda Virus Research Institute, Entebbe, Uganda;
**Faculty of Medicine, Makerere University College of Health Sciences, Kampala, Uganda;
††Columbia University, Mailman School of Public Health, New York, NY; and
‡‡Johns Hopkins Center for Global Health, Baltimore, MD.
Correspondence to: Dr Johan K. Sandberg, Department of Medicine, Center for Infectious Medicine, F59, Karolinska Institutet, Karolinska University Hospital Huddinge, 14186 Stockholm, Sweden (e-mail: email@example.com).
Primary support was provided by a cooperative agreement (W81XWH-07-2-0067) between the Henry M. Jackson Foundation for the Advancement of Military Medicine, Inc, and the US Department of Defense. Data collection was supported, in part, by grants R01 A134826 and R01 A134265 from the National Institute of Allergy and Infectious Diseases (NIAID); grant 5P30HD06826 from the National Institute of Child and Health Development; grant 5D43TW00010 from the Fogarty Foundation; and National Institutes of Health (NIH) grant R01 A134826. Additional support was provided by the Swedish Research Council, the Swedish Cancer Foundation, the Stockholm County Council, Karolinska Institutet, and the Division of Intramural Research, NIAID, NIH.
The authors have no conflicts of interest to disclose.
Received November 02, 2012
Accepted January 31, 2013