The DOI matches its Crossref record; 23 of the 23 references it cites were found in a registry or an index.
Adaptation of HIV-1 to human leukocyte antigen class I
Open accessAbstract
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 infection. 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.
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Cites
Approximate is Better than “Exact” for Interval Estimation of Binomial Proportions
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Self-citationCD8+ T-cell responses to different HIV proteins have discordant associations with viral load
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Self-citationHIV evolution: CTL escape mutation and reversion after transmission
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Self-citationDominant influence of HLA-B in mediating the potential co-evolution of HIV and HLA
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Self-citationEvidence of HIV-1 Adaptation to HLA-Restricted Immune Responses at a Population Level
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Self-citationEvolution and transmission of stable CTL escape mutations in HIV infection
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Self-citationImpact of MHC class I diversity on immune control of immunodeficiency virus replication
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Cited by
Van den Bergh, R., Morin, S., Sass, H. J., Grzesiek, S., Vekemans, M., Florence, E., Thanh Thi Tran, H., Imiru, R. G., Heyndrickx, L., Vanham, G., et al. (2012) · PLoS ONE · doi:10.1371/journal.pone.0035074 · Cited by 40
Metadata
- Authors
- Kawashima, Y., Pfafferott, K., Frater, J., Matthews, P., Payne, R., Addo, M., Gatanaga, H., Fujiwara, M., Hachiya, A., Koizumi, H., Kuse, N., Oka, S., Duda, A., Prendergast, A., Crawford, H., Leslie, A., Brumme, Z., Brumme, C., Allen, T., Brander, C., Kaslow, R., Tang, J., Hunter, E., Allen, S., Mulenga, J., Branch, S., Roach, T., John, M., Mallal, S., Ogwu, A., Shapiro, R., Prado, J. G., Fidler, S., Weber, J., Pybus, O. G., Klenerman, P., Ndung’u, T., Phillips, R., Heckerman, D., Harrigan, P. R., Walker, B. D., Takiguchi, M., & Goulder, P.
- Venue
- Nature
- Published
- 2009-02-25
- Volume
- 458
- Issue
- 7238
- Pages
- 641-645
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W2069926681
- Cited by
- 466
- References
- 23
- FWCI
- 21.78
- Type
- journal article
- Language
- en
- Open access
- green
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- Kawashima, Y., Pfafferott, K., Frater, J., Matthews, P., Payne, R., Addo, M., Gatanaga, H., Fujiwara, M., Hachiya, A., Koizumi, H., Kuse, N., Oka, S., Duda, A., Prendergast, A., Crawford, H., Leslie, A., Brumme, Z., Brumme, C., Allen, T., . . . Goulder, P. (2009). Adaptation of HIV-1 to human leukocyte antigen class I. Nature. https://doi.org/10.1038/nature07746
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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