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人类和猿猴免疫缺陷病毒序列集的网络分析揭示了大量重组,导致途径缩短。

Network analysis of human and simian immunodeficiency virus sequence sets reveals massive recombination resulting in shorter pathways.

作者信息

Wain-Hobson Simon, Renoux-Elbé Céline, Vartanian Jean-Pierre, Meyerhans Andreas

机构信息

Unité de Rétrovirologie Moléculaire, Institut Pasteur, F-75724 Paris cedex 15, France.

Department of Virology, University of the Saarland, D-66421 Homburg, Germany.

出版信息

J Gen Virol. 2003 Apr;84(Pt 4):885-895. doi: 10.1099/vir.0.18894-0.

DOI:10.1099/vir.0.18894-0
PMID:12655089
Abstract

The intrinsic recombination rate of human immunodeficiency virus (HIV) exceeds the point mutation rate by a factor of 10. As the majority of infected cells in vivo harbour multiple proviruses, the stage is set for rampant recombination. Therefore, it may be presumed that phylogenic relationships and mutation frequencies will probably be affected by recombination. However, the proportion of homoplasies arising from recombination and mutation is not known. By studying the evolution of the hypervariable regions of the simian immunodeficiency virus envelope gene among four macaques, it is shown that homoplasies arise more from recombination than from point mutation. When recombination is accounted for, the minimum number of substitutions in a sequence set may be reduced by as much as 45 %. In fact, the true number of point mutations in a set of HIV sequences tends to the number of discrete substitutions. Hence, lineages are younger than anticipated previously, although not in proportion to the ratio of the intrinsic recombination/point mutation rate. Recombination also inflates codon polymorphisms.

摘要

人类免疫缺陷病毒(HIV)的固有重组率比点突变率高出10倍。由于体内大多数受感染细胞含有多个前病毒,这为猖獗的重组创造了条件。因此,可以推测系统发育关系和突变频率可能会受到重组的影响。然而,由重组和突变产生的平行进化性状的比例尚不清楚。通过研究四只猕猴体内猿猴免疫缺陷病毒包膜基因高变区的进化,结果表明,平行进化性状更多地源于重组而非点突变。当考虑到重组时,序列集中替换的最小数量可能会减少多达45%。事实上,一组HIV序列中真正的点突变数量趋向于离散替换的数量。因此,谱系比之前预期的要年轻,尽管与固有重组/点突变率的比例不成正比。重组也会使密码子多态性膨胀。

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