Loss of linkage disequilibrium and accelerated protein divergence in duplicated cytomegalovirus chemokine genes

Human CMV (hCMV) encodes several captured chemokine ligand and chemokine receptor genes that may play a role in immune evasion. The adjacent viral alpha-chemokine genes UL146 and UL147 appear to have duplicated subsequent to a recent gene capture event. Sequence data from multiple hCMV isolates sugg...

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Bibliographic Details
Published in:Virus genes 2005-08, Vol.31 (1), p.65-72
Main Authors: Arav-Boger, Ravit, Zong, Jian-Chao, Foster, Charles B
Format: Article
Language:English
Subjects:
Animals
Chemokines - genetics
Cytomegalovirus
Cytomegalovirus - classification
Cytomegalovirus - genetics
Cytomegalovirus - isolation & purification
Cytomegalovirus Infections
Evolution, Molecular
Gene Duplication
Genetic Variation
Human cytomegalovirus
Humans
Linkage Disequilibrium
Molecular Sequence Data
Phylogeny
Viral Proteins - genetics
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Summary:Human CMV (hCMV) encodes several captured chemokine ligand and chemokine receptor genes that may play a role in immune evasion. The adjacent viral alpha-chemokine genes UL146 and UL147 appear to have duplicated subsequent to a recent gene capture event. Sequence data from multiple hCMV isolates suggest accelerated protein evolution in one of the paralogues, UL146. Extensive sequence variation was noted throughout the more rapidly evolving paralogue, although significant variation was also observed within the more slowly evolving gene, especially within a region corresponding to a possible signal peptide. In contrast to the haplotype structure observed for other hCMV genes, the distribution of nucleotide variants indicates a marked loss of linkage disequilibrium within UL146 and to a lesser extent UL147. Despite evidence of accelerated protein evolution, the rate of nonsynonymous to synonymous substitutions (d(N)/d(S)) in the more rapidly evolving paralogue was not indicative of neutral evolution, but of moderate purifying selection. The data presented here provides a unique opportunity to study the mechanisms by which a recently duplicated pair of genes has diverged and suggests a role for recombination.
ISSN:0920-8569
1572-994X
DOI:10.1007/s11262-005-2201-3