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

Molecular mechanisms of FIV infection.

Author information

1
Department of Molecular Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, United States. jelder@scripps.edu

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.

PMID:
18289701
PMCID:
PMC2409060
DOI:
10.1016/j.vetimm.2008.01.007
[Indexed for MEDLINE]
Free PMC Article

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