학술논문

Comparative requirements for the restriction of retrovirus infection by TRIM5[alpha] and TRIMCyp
Document Type
Report
Author abstract
Source
Virology. Dec 20, 2007, Vol. 369 Issue 2, p400, 11 p.
Subject
HIV (Viruses) -- Health aspects
HIV (Viruses) -- Comparative analysis
Language
English
ISSN
0042-6822
Abstract
To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.virol.2007.08.032 Byline: Felipe Diaz-Griffero (a), Alak Kar (a), Mark Lee (a), Matthew Stremlau (a), Eric Poeschla (b), Joseph Sodroski (a)(c) Keywords: Restriction factors; Retrovirus; Uncoating; Human immunodeficiency virus Abstract: The restriction factors, TRIM5[alpha] in most primates and TRIMCyp in owl monkeys, block infection of various retroviruses soon after virus entry into the host cell. Rhesus monkey TRIM5[alpha] (TRIM5[alpha].sub.rh) inhibits human immunodeficiency virus (HIV-1) and feline immunodeficiency virus (FIV) more potently than human TRIM5[alpha] (TRIM5[alpha].sub.hu). TRIMCyp restricts infection of HIV-1, simian immunodeficiency virus of African green monkeys (SIV.sub.agm) and FIV. Early after infection, TRIMCyp, like TRIM5[alpha].sub.rh and TRIM5[alpha].sub.hu, decreased the amount of particulate viral capsid in the cytosol of infected cells. The requirements for the TRIMCyp and TRIM5[alpha] domains in restricting different retroviruses were investigated. Potent restriction of FIV by TRIMCyp occurred in the complete absence of RING and B-box 2 domains; by contrast, efficient FIV restriction by TRIM5[alpha].sub.rh required these domains. Variable region 1 of the TRIM5[alpha].sub.rh B30.2 domain contributed to the potency of HIV-1, FIV and equine infectious anemia virus restriction. Thus, although differences exist in the requirements of TRIMCyp and TRIM5[alpha] for RING/B-box 2 domains, both restriction factors exhibit mechanistic similarities. Author Affiliation: (a) Department of Cancer Immunology and AIDS, Dana-Farber Cancer Institute, Department of Pathology, Division of AIDS, Harvard Medical School, Boston, MA 02115, USA (b) Molecular Medicine Program, Mayo Clinic College of Medicine, Rochester, MN 55905, USA (c) Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA 02115, USA Article History: Received 7 June 2007; Revised 27 June 2007; Accepted 30 August 2007