Molecular mechanisms of FIV infection

被引:34
作者
Elder, John H. [1 ]
Sundstrom, Magnus [1 ]
de Rozieres, Sohela [2 ]
de Parseval, Aymeric [3 ]
Grant, Chris K. [4 ]
Lin, Ying-Chuan [1 ]
机构
[1] Scripps Res Inst, Dept Mol Biol, La Jolla, CA 92037 USA
[2] Biomatrica, San Diego, CA 92121 USA
[3] Publ Hlth Res Inst, Newark, NJ 07103 USA
[4] Custom Monoclonals Int, W Sacramento, CA 95691 USA
关键词
feline immunodeficiency virus; receptor; CD134; CXCR4;
D O I
10.1016/j.vetimm.2008.01.007
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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. (C) 2008 Elsevier B.V. All rights reserved.
引用
收藏
页码:3 / 13
页数:11
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