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Journal of Virology, November 2007, p. 12666-12669, Vol. 81, No. 22
0022-538X/07/$08.00+0 doi:10.1128/JVI.01450-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Partners AIDS Research Center, Massachusetts General Hospital and Harvard University Center for AIDS Research, Boston, Massachusetts,1 Fundació irsiCaixa, Hospital Universitari Germans Trias i Pujol, Barcelona, Spain,2 Institució Catalana de Recerca i Estudis Avançats (ICREA), Barcelona, Spain,3 Howard Hughes Medical Institute, Chevy Chase, Maryland4
Received 3 July 2007/ Accepted 20 August 2007
Human immunodeficiency virus type 1 (HIV-1) cytotoxic T-lymphocyte escape mutations represent both a major reason for loss of HIV immune control and a considerable challenge for HIV-1 vaccine design. Previous data suggest that initial HIV-1-specific CD8+ T-cell responses are determined largely by viral and host genetics, but the mechanisms influencing the subsequent viral evolution are unclear. Here, we show a random recruitment of T-cell receptor (TCR) alpha and beta clonotypes of the initial HIV-1-specific CD8+ T cells during primary infection in two genetically identical twins infected simultaneously with the same virus, suggesting that stochastic TCR recruitment of HIV-1-specific CD8+ T cells contributes to the diverse and unpredictable HIV-1 sequence evolution.
Published ahead of print on 5 September 2007.
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