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Journal of Virology, June 2006, p. 6056-6060, Vol. 80, No. 12
0022-538X/06/$08.00+0     doi:10.1128/JVI.02119-05
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Human Leukocyte Antigen B58 Supertype and Human Immunodeficiency Virus Type 1 Infection in Native Africans

Aleksandr Lazaryan,1 Elena Lobashevsky,1 Joseph Mulenga,4 Etienne Karita,5 Susan Allen,6 Jianming Tang,2 and Richard A. Kaslow1,2,3*

Departments of Epidemiology,1 Medicine,2 Microbiology, University of Alabama at Birmingham, Birmingham, Alabama,3 National Blood Transfusion Service, Lusaka, Zambia,4 Project San Francisco, Kigali, Rwanda,5 Department of Global Health, Emory University, Atlanta, Georgia6

Received 8 October 2005/ Accepted 5 April 2006

Human leukocyte antigen (HLA) class I alleles can be grouped into supertypes according to their shared peptide binding properties. We examined alleles of the HLA-B58 supertype (B58s) in treatment-naïve human immunodeficiency virus type 1 (HIV-1)-seropositive Africans (423 Zambians and 202 Rwandans). HLA-B and HLA-C alleles were resolved to four digits by a combination of molecular methods, and their respective associations with outcomes of HIV-1 infection were analyzed by statistical procedures appropriate for continuous or categorical data. The effects of the individual alleles on natural HIV-1 infection were heterogeneous. In HIV-1 subtype C-infected Zambians, the mean viral load (VL) was lower among B*5703 (P = 0.01) or B*5703-Cw*18 (P < 0.001) haplotype carriers and higher among B*5802 (P = 0.02) or B*5802-Cw*0602 (P = 0.03) carriers. The B*5801-Cw*03 haplotype showed an association with low VL (P = 0.05), whereas B*5801 as a whole did not. Rwandans with HIV-1 subtype A infection showed associations of B*5703 and B*5802 with slow (P = 0.06) and rapid (P = 0.003) disease progression, respectively. In neither population were B*1516-B*1517 alleles associated with more favorable responses. Overall, B58s alleles, individually or as part of an HLA-B-HLA-C haplotype, appeared to have a distinctive impact on HIV-1 infection among native Africans. As presently defined, B58s alleles cannot be considered uniformly protective against HIV/AIDS in every population.

* Corresponding author. Mailing address: Department of Epidemiology, University of Alabama at Birmingham, 220A Ryals Bldg., 1665 University Blvd, Birmingham, AL 35294. Phone: (205) 975-8698. Fax: (205) 934-8665. E-mail: rkaslow{at}uab.edu.

Journal of Virology, June 2006, p. 6056-6060, Vol. 80, No. 12
0022-538X/06/$08.00+0     doi:10.1128/JVI.02119-05
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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