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猫免疫缺陷病毒感染的分子机制。

Molecular mechanisms of FIV infection.

作者信息

Elder John H, Sundstrom Magnus, de Rozieres Sohela, de Parseval Aymeric, Grant Chris K, Lin Ying-Chuan

机构信息

Department of Molecular Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, United States.

出版信息

Vet Immunol Immunopathol. 2008 May 15;123(1-2):3-13. doi: 10.1016/j.vetimm.2008.01.007. Epub 2008 Jan 19.

Abstract

Feline immunodeficiency virus (FIV) is an important viral pathogen worldwide in the domestic cat, which is the smallest animal model for the study of natural lentivirus infection. Thus, understanding the molecular mechanisms by which FIV carries out its life cycle and causes an acquired immune deficiency syndrome (AIDS) in the cat is of high priority. FIV has an overall genome size similar to HIV, the causative agent of AIDS in man, and shares with the human virus genomic features that may serve as common targets for development of broad-based intervention strategies. Specific targets include enzymes encoded by the two lentiviruses, such as protease (PR), reverse transcriptase (RT), RNAse H, and integrase (IN). In addition, both FIV and HIV encode Vif and Rev elements essential for virus replication and also share the use of the chemokine receptor CXCR4 for entry into the host cell. The following review is a brief overview of the current state of characterization of the feline/FIV model and development of its use for generation and testing of anti-viral agents.

摘要

猫免疫缺陷病毒(FIV)是全球家猫中一种重要的病毒病原体,家猫是研究自然慢病毒感染的最小动物模型。因此,了解FIV进行其生命周期并在猫中引起获得性免疫缺陷综合征(AIDS)的分子机制是当务之急。FIV的总体基因组大小与人类AIDS病原体HIV相似,并且与人类病毒共享可能作为广泛干预策略开发共同靶点的基因组特征。具体靶点包括两种慢病毒编码的酶,如蛋白酶(PR)、逆转录酶(RT)、核糖核酸酶H和整合酶(IN)。此外,FIV和HIV都编码病毒复制所必需的Vif和Rev元件,并且在进入宿主细胞时都使用趋化因子受体CXCR4。以下综述简要概述了猫/FIV模型的表征现状及其在抗病毒药物生成和测试中的应用发展。

相似文献

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Molecular mechanisms of FIV infection.猫免疫缺陷病毒感染的分子机制。
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