Type I IFN - A blunt spear in fighting HIV-1 infection

被引:23
作者
Acchioni, Chiara [1 ]
Marsili, Giulia [1 ]
Perrotti, Edvige [1 ]
Remoli, Anna Lisa [1 ]
Sgarbanti, Marco [1 ]
Battistini, Angela [1 ]
机构
[1] Ist Super Sanita, Dept Infect Parasit & Immune Mediated Dis, I-00161 Rome, Italy
关键词
HIV-1; Type I interferon; Innate immune sensing; Interferon Regulatory Factors; HIV-1 immune activation; IMMUNODEFICIENCY-VIRUS TYPE-1; PLASMACYTOID DENDRITIC CELLS; INTERFERON REGULATORY FACTOR; AICARDI-GOUTIERES-SYNDROME; PATTERN-RECOGNITION RECEPTORS; INNATE IMMUNE RECOGNITION; HOST RESTRICTION FACTOR; TOLL-LIKE RECEPTORS; GMP-AMP SYNTHASE; CD4(+) T-CELLS;
D O I
10.1016/j.cytogfr.2014.10.004
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
For more than 50 years, Type I Interferon (IFN) has been recognized as critical in controlling viral infections. IFN is produced downstream germ-line encoded pattern recognition receptors (PRRs) upon engagement by pathogen-associated molecular patterns (PAMPs). As a result, hundreds of different interferon-stimulated genes (ISGs) are rapidly induced, acting in both autocrine and paracrine manner to build a barrier against viral replication and spread. ISGs encode proteins with direct antiviral and immunomodulatory activities affecting both innate and adaptive immune responses. During infection with viruses, as HIV-1, that can establish a persistent infection, IFN although produced, is not able to block the initial infection and a chronic IFN-mediated immune activation/inflammation becomes a pathogenic mechanism of disease progression. This review will briefly summarize when and how IFN is produced during HIV-1 infection and the way this innate immune response is manipulated by the virus to its own advantage to drive chronic immune activation and progression to AIDS. (C) 2014 Elsevier Ltd. All rights reserved.
引用
收藏
页码:143 / 158
页数:16
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