Induction and Evasion of Innate Antiviral Responses by Hepatitis C Virus

被引：79

作者：

Lemon, Stanley M. ^{[1
]}

机构：

[1] Univ N Carolina, Inflammatory Dis Inst, Lineberger Comprehens Canc Ctr, Div Infect Dis,Dept Med,Ctr Translat Immunol, Chapel Hill, NC 27599 USA

来源：

JOURNAL OF BIOLOGICAL CHEMISTRY | 2010年 / 285卷 / 30期

关键词：

DOUBLE-STRANDED-RNA; TOLL-LIKE RECEPTOR-3; NF-KAPPA-B; INTERFERON REGULATORY FACTOR-3; PLASMACYTOID DENDRITIC CELLS; NONSTRUCTURAL PROTEIN 5A; RIG-I; VIRAL-INFECTION; ADAPTER PROTEIN; TRANSCRIPTION FACTORS;

D O I：

10.1074/jbc.R109.099556

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：

Persistent hepatitis C virus infection is associated with progressive hepatic fibrosis and liver cancer. Acute infection evokes several distinct innate immune responses, but these are partially or completely countered by the virus. Hepatitis C virus proteins serve dual functions in replication and immune evasion, acting to disrupt cellular signaling pathways leading to interferon synthesis, subvert Jak-STAT signaling to limit expression of interferon-stimulated genes, and block antiviral activities of interferon-stimulated genes. The net effect is a multilayered evasion of innate immunity, which negatively influences the subsequent development of antigen-specific adaptive immunity, thereby contributing to virus persistence and resistance to therapy.

引用

页码：22739 / 22745

页数：7

共 100 条

[81] Recognition of 5′ Triphosphate by RIG-I Helicase Requires Short Blunt Double-Stranded RNA as Contained in Panhandle of Negative-Strand Virus [J].

Schlee, Martin ;

Roth, Andreas ;

Hornung, Veit ;

Hagmann, Cristina Amparo ;

Wimmenauer, Vera ;

Barchet, Winfried ;

Coch, Christoph ;

Janke, Markus ;

Mihailovic, Aleksandra ;

Wardle, Greg ;

Juranek, Stefan ;

Kato, Hiroki ;

Kawai, Taro ;

Poeck, Hendrik ;

Fitzgerald, Katherine A. ;

Takeuchi, Osamu ;

Akira, Shizuo ;

Tuschl, Thomas ;

Latz, Eicke ;

Ludwig, Janos ;

Hartmann, Gunther .

IMMUNITY, 2009, 31 (01) :25-34

[82] Toll-like receptors and adaptor molecules in liver disease: Update [J].

Seki, Ekihiro ;

Brenner, David A. .

HEPATOLOGY, 2008, 48 (01) :322-335

[83] Identification and characterization of MAVS, a mitochondrial antiviral signaling protein that activates NF-κB and IRF3 [J].

Seth, RB ;

Sun, LJ ;

Ea, CK ;

Chen, ZJJ .

CELL, 2005, 122 (05) :669-682

[84] Hepatitis C: recent successes and continuing challenges in the development of improved treatment modalities [J].

Shimakami, Tetsuro ;

Lanford, Robert E. ;

Lemon, Stanley M. .

CURRENT OPINION IN PHARMACOLOGY, 2009, 9 (05) :537-544

[85] Translational insensitivity to potent activation of PKR by HCV IRES RNA [J].

Shimoike, Takashi ;

McKenna, Sean A. ;

Lindhout, Darrin A. ;

Puglisi, Joseph D. .

ANTIVIRAL RESEARCH, 2009, 83 (03) :228-237

[86]

Shin EC, 2007, J INTERF CYTOK RES, V27, P985, DOI 10.1089/jir.2007.0039

[87] Regulating intracellular antiviral defense and permissiveness to hepatitis C virus RNA replication through a cellular RNA helicase, RIG-I [J].

Stumper, R ;

Loo, YM ;

Foy, E ;

Li, K ;

Yoneyama, M ;

Fujita, T ;

Lemon, SM ;

Gale, M .

JOURNAL OF VIROLOGY, 2005, 79 (05) :2689-2699

[88] Hepatitis C virus NS5A protein interacts with 2′,5′-oligoadenylate synthetase and inhibits antiviral activity of IFN in an IFN sensitivity-determining region-independent manner [J].

Taguchi, T ;

Nagano-Fujii, M ;

Akutsu, M ;

Kadoya, H ;

Ohgimoto, S ;

Ishido, S ;

Hotta, H .

JOURNAL OF GENERAL VIROLOGY, 2004, 85 :959-969

[89] Plasmacytoid dendritic cells sense hepatitis C virus-infected cells, produce interferon, and inhibit infection [J].

Takahashi, Ken ;

Asabe, Shinichi ;

Wieland, Stefan ;

Garaigorta, Urtzi ;

Gastaminza, Pablo ;

Isogawa, Masanori ;

Chisari, Francis V. .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2010, 107 (16) :7431-7436

[90] Innate immunity to virus infection [J].

Takeuchi, Osamu ;

Akira, Shizuo .

IMMUNOLOGICAL REVIEWS, 2009, 227 :75-86

← 1 2 3 4 5 6 7 8 9 10 →