ArticleBMC evolutionary biology2009
The distribution of CTL epitopes in HIV-1 appears to be random, and similar to that of other proteomes.
Article in BMC evolutionary biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Predicted MHC peptide binding promiscuity explains MHC class I 'hotspots' of antigen presentation defined by mass spectrometry eluted ligand data.Immunology · 2018Article
- Analysis of HIV-1 envelope evolution suggests antibody-mediated selection of common epitopes among Chinese former plasma donors from a narrow-source outbreak.Scientific reports · 2018Article
- Key role of human leukocyte antigen in modulating human immunodeficiency virus progression: An overview of the possible applications.World journal of virology · 2015Review
- Article
- Sequence- and interactome-based prediction of viral protein hotspots targeting host proteins: a case study for HIV Nef.PloS one · 2011Article
- Article
- HLA class I binding of HBZ determines outcome in HTLV-1 infection.PLoS pathogens · 2010Article
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHIV-1 viruses are highly capable of mutating their proteins to escape the presentation of CTL epitopes in their current host. Upon transmission to another host, some escape mutations revert, but other remain stable in the virus sequence for at least several years. Depending on the rate of accumulation and reversion of escape mutations, HIV-1 could reach a high level of adaptation to the human population. Yusim et. al. hypothesized that the apparent clustering of CTL epitopes in the conserved regions of HIV-1 proteins could be an evolutionary signature left by large-scale adaptation of HIV-1 to its human/simian host.
resultsIn this paper we quantified the distribution of CTL epitopes in HIV-1 and found that that in 99% of the HIV-1 protein sequences, the epitope distribution was indistinguishable from random. Similar percentages were found for HCV, Influenza and for three eukaryote proteomes (Human, Drosophila, Yeast).
conclusionWe conclude that CTL epitopes in HIV-1 are randomly distributed, and that this distribution is similar to the distribution of CTL epitopes in proteins from other proteomes. Therefore, the visually apparent clustering of CTL epitopes in epitope maps should not be interpreted as a signature of a past large-scale adaptation of HIV-1 to the human cellular immune response.
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