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


RESULTS
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).


CONCLUSIONS
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.
Schmid
Boris V
BV
Theoretical Biology, Utrecht University, the Netherlands. boris.schmid@gmail.com
Keşmir
Can
C
de Boer
Rob J
RJ
D000220:Adaptation, Biological / Q000235:genetics; D016000:Cluster Analysis; D018604:Epitope Mapping; D018984:Epitopes, T-Lymphocyte / Q000235:genetics*; D019143:Evolution, Molecular; D015497:HIV-1 / Q000235:genetics*; D020543:Proteome / Q000235:genetics*; D020539:Sequence Analysis, Protein
D018984:Epitopes, T-Lymphocyte; D020543:Proteome