The distribution of CTL epitopes in HIV-1 appears to be random, and similar to that of other proteomes

<p>Abstract</p> <p>Background</p> <p>HIV-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 seque...

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Main Authors: Keşmir Can, Schmid Boris V, de Boer Rob J
Format: Article
Language:English
Published: BMC 2009-08-01
Series:BMC Evolutionary Biology
Online Access:http://www.biomedcentral.com/1471-2148/9/184
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spelling doaj-7889f38ca7d7468eb90f64a434374b452021-09-02T08:50:16ZengBMCBMC Evolutionary Biology1471-21482009-08-019118410.1186/1471-2148-9-184The distribution of CTL epitopes in HIV-1 appears to be random, and similar to that of other proteomesKeşmir CanSchmid Boris Vde Boer Rob J<p>Abstract</p> <p>Background</p> <p>HIV-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.</p> <p>Results</p> <p>In 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).</p> <p>Conclusion</p> <p>We 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.</p> http://www.biomedcentral.com/1471-2148/9/184
collection DOAJ
language English
format Article
sources DOAJ
author Keşmir Can
Schmid Boris V
de Boer Rob J
spellingShingle Keşmir Can
Schmid Boris V
de Boer Rob J
The distribution of CTL epitopes in HIV-1 appears to be random, and similar to that of other proteomes
BMC Evolutionary Biology
author_facet Keşmir Can
Schmid Boris V
de Boer Rob J
author_sort Keşmir Can
title The distribution of CTL epitopes in HIV-1 appears to be random, and similar to that of other proteomes
title_short The distribution of CTL epitopes in HIV-1 appears to be random, and similar to that of other proteomes
title_full The distribution of CTL epitopes in HIV-1 appears to be random, and similar to that of other proteomes
title_fullStr The distribution of CTL epitopes in HIV-1 appears to be random, and similar to that of other proteomes
title_full_unstemmed The distribution of CTL epitopes in HIV-1 appears to be random, and similar to that of other proteomes
title_sort distribution of ctl epitopes in hiv-1 appears to be random, and similar to that of other proteomes
publisher BMC
series BMC Evolutionary Biology
issn 1471-2148
publishDate 2009-08-01
description <p>Abstract</p> <p>Background</p> <p>HIV-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.</p> <p>Results</p> <p>In 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).</p> <p>Conclusion</p> <p>We 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.</p>
url http://www.biomedcentral.com/1471-2148/9/184
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