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Journal of Virology, February 2007, p. 1619-1631, Vol. 81, No. 4
0022-538X/07/$08.00+0     doi:10.1128/JVI.01580-06

Mutually Exclusive T-Cell Receptor Induction and Differential Susceptibility to Human Immunodeficiency Virus Type 1 Mutational Escape Associated with a Two-Amino-Acid Difference between HLA Class I Subtypes{triangledown}

Xu G. Yu,1,{dagger} Mathias Lichterfeld,1,{dagger} Senica Chetty,2,{dagger} Katie L. Williams,1 Stanley K. Mui,1 Toshiyuki Miura,1 Nicole Frahm,1 Margaret E. Feeney,1 Yanhua Tang,1 Florencia Pereyra,1 Montiago X. LaBute,3 Katja Pfafferott,4 Alisdair Leslie,4 Hayley Crawford,4 Rachel Allgaier,1 William Hildebrand,5 Richard Kaslow,6 Christian Brander,1 Todd M. Allen,1 Eric S. Rosenberg,1 Photini Kiepiela,2 Madhu Vajpayee,7 Paul A. Goepfert,6 Marcus Altfeld,1 Philip J. R. Goulder,1,2,4 and Bruce D. Walker1,2,8*

Partners AIDS Research Center, Massachusetts General Hospital and Harvard University Center for AIDS Research, Boston, Massachusetts,1 HIV Pathogenesis Program, The Doris Duke Medical Research Institute, University of KwaZulu-Natal, Durban, South Africa,2 Theoretical Biology and Biophysics Group, Theoretical Division, Los Alamos National Laboratory, Los Alamos, New Mexico,3 Department of Paediatrics, Nuffield Department of Medicine, Peter Medawar Building for Pathogen Research, University of Oxford, Oxford, United Kingdom,4 University of Oklahoma Health Science Center, Oklahoma City, Oklahoma,5 University of Alabama at Birmingham, Birmingham, Alabama,6 All India Institute for Medical Sciences, New Delhi, India,7 Howard Hughes Medical Institute, Chevy Chase, Maryland8

Received 24 July 2006/ Accepted 15 November 2006

The relative contributions of HLA alleles and T-cell receptors (TCRs) to the prevention of mutational viral escape are unclear. Here, we examined human immunodeficiency virus type 1 (HIV-1)-specific CD8+ T-cell responses restricted by two closely related HLA class I alleles, B*5701 and B*5703, that differ by two amino acids but are both associated with a dominant response to the same HIV-1 Gag epitope KF11 (KAFSPEVIPMF). When this epitope is presented by HLA-B*5701, it induces a TCR repertoire that is highly conserved among individuals, cross-recognizes viral epitope variants, and is rarely associated with mutational escape. In contrast, KF11 presented by HLA-B*5703 induces an entirely different, more heterogeneous TCR ß-chain repertoire that fails to recognize specific KF11 escape variants which frequently arise in clade C-infected HLA-B*5703+ individuals. These data show the influence of HLA allele subtypes on TCR selection and indicate that extensive TCR diversity is not a prerequisite to prevention of allowable viral mutations.

* Corresponding author. Mailing address: Partners AIDS Research Center, Massachusetts General Hospital, 149 13th Street, Room 5212, Charlestown, MA 02129. Phone: (617) 724-8332. Fax: (617) 726-4691. E-mail: bwalker{at}partners.org.

{triangledown} Published ahead of print on 22 November 2006.

{dagger} X.G.Y., M.L., and S.C. contributed equally to this work.

Journal of Virology, February 2007, p. 1619-1631, Vol. 81, No. 4
0022-538X/07/$08.00+0     doi:10.1128/JVI.01580-06




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