ArticleVirus genes2005
Loss of linkage disequilibrium and accelerated protein divergence in duplicated cytomegalovirus chemokine genes.
Article in Virus genes, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Evolution of the ability to modulate host chemokine networks via gene duplication in human cytomegalovirus (HCMV).Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2017Article
- Polymorphisms and features of cytomegalovirus UL144 and UL146 in congenitally infected neonates with hepatic involvement.PloS one · 2017Article
- Strain Variation and Disease Severity in Congenital Cytomegalovirus Infection: In Search of a Viral Marker.Infectious disease clinics of North America · 2015Review
- Extensive genome-wide variability of human cytomegalovirus in congenitally infected infants.PLoS pathogens · 2011Article
- Detection of a single identical cytomegalovirus (CMV) strain in recently seroconverted young women.PloS one · 2011Article
- Sequences of complete human cytomegalovirus genomes from infected cell cultures and clinical specimens.The Journal of general virology · 2010Article
- Feeling manipulated: cytomegalovirus immune manipulation.Virology journal · 2009Article
- Genotypic analysis of two hypervariable human cytomegalovirus genes.Journal of medical virology · 2008Article
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- Analysis of the human cytomegalovirus genomic region from UL146 through UL147A reveals sequence hypervariability, genotypic stability, and overlapping transcripts.Virology journal · 2006Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.