Isolation and phylogeny of endogenous retrovirus sequences belonging to the HERV-W family in primates

被引:59
|
作者
Kim, HS
Takenaka, O
Crow, TJ [1 ]
机构
[1] Univ Oxford, Warneford Hosp, Dept Psychiat, POWIC, Oxford OX3 7JX, England
[2] Kyoto Univ, Primate Res Inst, Dept Cellular & Mol Biol, Inuyama, Aichi 484, Japan
来源
JOURNAL OF GENERAL VIROLOGY | 1999年 / 80卷
关键词
D O I
10.1099/0022-1317-80-10-2613
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
An investigation was undertaken of primate pol gene sequences from a novel endogenous retrovirus family, ERV-W, related to a new human endogenous retrovirus family (HERV-W) that includes multiple sclerosis-associated retrovirus (MSRV) sequences identified in particles recovered from monocyte cultures from patients with multiple sclerosis. The pol gene sequences of the ERV-W family were detected in hominoids and Old World monkeys, but not in New World monkeys, whereas ERV-W long terminal repeat-like elements were detected in all primates (hominoids, Old World monkeys and New World monkeys). Thirty-two pol gene sequences from hominoids and Old World monkeys showed a high degree of sequence identity to MSRV and other HERV-W sequences. Phylogenetic analysis indicated close relationships of pol gene sequences across primate species. The analysis suggests that the ERV-W family has evolved independently but in constrained patterns ('parallel evolution') in different primate species, including man. The ratio of synonymous to non-synonymous substitutions indicated that negative selective pressure is acting on CHW1-1 from chimpanzee, HBW6-6 from baboon and HWX5 from man, sequences that have no disruption by point mutation or insertions/deletions. Therefore, these pol gene sequences could be associated with an active provirus in primates. The findings indicate that the ERV-W family has continued to evolve in the course of the primate radiation and may include members with a capacity to influence gene function and possibly cause disease.
引用
收藏
页码:2613 / 2619
页数:7
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