@article{kawashima2009adaptation,
author = {Kawashima, Yuka and Pfafferott, Katja and Frater, John and Matthews, Philippa and Payne, Rebecca and Addo, Marylyn and Gatanaga, Hiroyuki and Fujiwara, Mamoru and Hachiya, Atsuko and Koizumi, Hirokazu and Kuse, Nozomi and Oka, Shinichi and Duda, Anna and Pendergast, Andrew and Crawford, Hayley and Leslie, Alasdair and Brumme, Zabrina and Brumme, Chanson and Allen, Todd and Brander, Christian and Kaslow, Richard and Tang, James and Hunter, Eric and Allen, Susan and Mulenga, Joseph and Branch, Songee and Roach, Tim and John, Mina and Mallal, Simon and Ogwu, Anthony and Shapiro, Roger and Prado, Julia G. and Fidler, Sarah and Weber, Jonathan and Pybus, Oliver G. and Klenerman, Paul and Ndung'u, Thumbi and Phillips, Rodney and Heckerman, David and Harrigan, P. Richard and Walker, Bruce D. and Takiguchi, Masafumi and Goulder, Philip},
title = {Adaptation of HIV-1 to Human Leukocyte Antigen Class I},
year = {2009},
month = {April},
abstract = {The rapid and extensive spread of the human immunodeficiency virus (HIV) epidemic provides a rare opportunity to witness host–pathogen co-evolution involving humans. A focal point is the interaction between genes encoding human leukocyte antigen (HLA) and those encoding HIV proteins. HLA molecules present fragments (epitopes) of HIV proteins on the surface of infected cells to enable immune recognition and killing by CD8+ T cells; particular HLA molecules, such as HLA-B*57, HLA-B*27 and HLA-B*51, are more likely to mediate successful control of HIV infection1. Mutation within these epitopes can allow viral escape from CD8+ T-cell recognition. Here we analysed viral sequences and HLA alleles from >2,800 subjects, drawn from 9 distinct study cohorts spanning 5 continents. Initial analysis of the HLA-B*51-restricted epitope, TAFTIPSI (reverse transcriptase residues 128–135), showed a strong correlation between the frequency of the escape mutation I135X and HLA-B*51 prevalence in the 9 study cohorts (P = 0.0001). Extending these analyses to incorporate other well-defined CD8+ T-cell epitopes, including those restricted by HLA-B*57 and HLA-B*27, showed that the frequency of these epitope variants (n = 14) was consistently correlated with the prevalence of the restricting HLA allele in the different cohorts (together, P < 0.0001), demonstrating strong evidence of HIV adaptation to HLA at a population level. This process of viral adaptation may dismantle the well-established HLA associations with control of HIV infection that are linked to the availability of key epitopes, and highlights the challenge for a vaccine to keep pace with the changing immunological landscape presented by HIV.},
url = {http://approjects.co.za/?big=en-us/research/publication/adaptation-hiv-1-human-leukocyte-antigen-class/},
pages = {641-645},
journal = {Nature},
volume = {458},
}