Truncation of TRIM5 in the Feliformia Explains the Absence of Retroviral Restriction in Cells of the Domestic Cat

被引:50
|
作者
McEwan, William A. [1 ]
Schaller, Torsten [2 ]
Ylinen, Laura M. [2 ]
Hosie, Margaret J. [1 ]
Towers, Greg J. [2 ]
Willett, Brian J. [1 ]
机构
[1] Univ Glasgow, Fac Vet Med, Inst Comparat Med, Retrovirus Res Lab, Glasgow G61 1QH, Lanark, Scotland
[2] UCL, Royal Free & Univ Coll Med Sch, Dept Infect, MRC Ctr Med Mol Virol, London, England
基金
英国生物技术与生命科学研究理事会; 英国惠康基金;
关键词
FELINE IMMUNODEFICIENCY VIRUS; PRIMATE TRIM5-ALPHA; CYCLOPHILIN-A; SIMIAN IMMUNODEFICIENCY; REVERSE TRANSCRIPTION; HIV-1; INFECTION; LEUKEMIA-VIRUS; MOTIF PROTEIN; B30.2; DOMAIN; GENE;
D O I
10.1128/JVI.00670-09
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
TRIM5 alpha mediates a potent retroviral restriction phenotype in diverse mammalian species. Here, we identify a TRIM5 transcript in cat cells with a truncated B30.2 capsid binding domain and ablated restrictive function which, remarkably, is conserved across the Feliformia. Cat TRIM5 displayed no restriction activity, but ectopic expression conferred a dominant negative effect against human TRIM5 alpha. Our findings explain the absence of retroviral restriction in cat cells and suggest that disruption of the TRIM5 locus has arisen independently at least twice in the Carnivora, with implications concerning the evolution of the host and pathogen in this taxon.
引用
收藏
页码:8270 / 8275
页数:6
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