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亲环素A和TRIMCyp逆转座在新大陆灵长类动物中的进化。

Evolution of cyclophilin A and TRIMCyp retrotransposition in New World primates.

作者信息

Ribeiro Ieda P, Menezes Albert N, Moreira Miguel A M, Bonvicino Cibele R, Seuánez Héctor N, Soares Marcelo A

机构信息

Departamento de Genética, Universidade Federal do Rio de Janeiro, CCS-bloco A-sala A2-121, Cidade Universitaria-Ilha do Fundão, 21949-570 Rio de Janeiro, Brazil.

出版信息

J Virol. 2005 Dec;79(23):14998-5003. doi: 10.1128/JVI.79.23.14998-15003.2005.

Abstract

Host cell factors modulate retroviral infections. Among those, cyclophilin A (CypA) promotes virus infectivity by facilitating virus uncoating or capsid unfolding or by preventing retroviral capsid interaction with cellular restriction factors. In Aotus species, a retrotransposed copy of CypA inserted into the tripartite motif 5 (TRIM5) gene encodes a fusion protein which may block human immunodeficiency virus type 1 by targeting the incoming virus to ubiquitin-ligated degradation or by interfering with normal uncoating of the incoming particle, rendering those monkeys resistant to infection. In this study, we have extensively analyzed representative specimens from all New World primate genera and shown that the retrotransposed CypA copy is only present in Aotus. We have shown that this inserted copy diverged from its original counterpart and that this occurred prior to Aotus radiation, although no positive selection was observed. Finally, our data underscores the need for a precise taxonomic identification of primate species used as models for retroviral infections and novel antiviral approaches.

摘要

宿主细胞因子可调节逆转录病毒感染。其中,亲环素A(CypA)通过促进病毒脱壳或衣壳解折叠,或通过阻止逆转录病毒衣壳与细胞限制因子相互作用来提高病毒感染性。在夜猴属物种中,插入到三联基序5(TRIM5)基因中的CypA逆转座拷贝编码一种融合蛋白,该蛋白可能通过将进入的病毒靶向泛素连接的降解过程或通过干扰进入颗粒的正常脱壳过程来阻断1型人类免疫缺陷病毒,使这些猴子对感染具有抗性。在本研究中,我们广泛分析了所有新大陆灵长类属的代表性标本,并表明逆转座的CypA拷贝仅存在于夜猴属中。我们已经表明,这个插入的拷贝与其原始对应物发生了分歧,并且这种分歧发生在夜猴属辐射之前,尽管未观察到正选择。最后,我们的数据强调了对用作逆转录病毒感染模型和新型抗病毒方法的灵长类物种进行精确分类鉴定的必要性。

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