Hepatitis C virus (HCV) employs multiple strategies to subvert the host innate antiviral response

被引:33
作者
Bode, Johannes G. [1 ]
Brenndoerfer, Erwin D. [1 ]
Haeussinger, Dieter [1 ]
机构
[1] Univ Dusseldorf, Univ Hosp, Dept Gastroenterol Hepatol & Infectiol, D-40225 Dusseldorf, Germany
关键词
hepatitis C; innate immunity; interferon signaling; pathogen-associated molecular pattern; pathogen recognition receptors; retinoic acid-inducible gene I;
D O I
10.1515/BC.2008.147
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
Hepatitis C virus (HCV) is a serious global health problem which accounts for approximately 40% of chronic liver diseases worldwide. HCV frequently establishes a persistent infection, although it is recognized and targeted by innate immunity as well as cellular and humoral immune mechanisms. This suggests that HCV has developed powerful strategies to escape elimination by innate and adaptive immunity. HCV-induced liver injury is thought to be mainly immune-mediated rather than due to direct cytopathic effects of the virus. Hence, therapeutic strategies should target those mechanisms favoring viral persistence since unspecific enhancement of host antiviral immunity may theoretically also promote liver injury. The present review summarizes our current understanding of how the hepatitis C virus interferes with the innate antiviral host-response to establish persistent infection.
引用
收藏
页码:1283 / 1298
页数:16
相关论文
共 179 条
[1]   Hepatitis C Lipo-Viro-Particle from Chronically Infected Patients Interferes with TLR4 Signaling in Dendritic Cell [J].
Agaugue, Sophie ;
Perrin-Cocon, Laure ;
Andre, Patrice ;
Lotteau, Vincent .
PLOS ONE, 2007, 2 (03)
[2]   Role of NK and NKT cells in the immunopathogenesis of HCV-induced hepatitis [J].
Ahmad, A ;
Alvarez, F .
JOURNAL OF LEUKOCYTE BIOLOGY, 2004, 76 (04) :743-759
[3]   Recognition of double-stranded RNA and activation of NF-κB by Toll-like receptor 3 [J].
Alexopoulou, L ;
Holt, AC ;
Medzhitov, R ;
Flavell, RA .
NATURE, 2001, 413 (6857) :732-738
[4]   Natural killer cells in viral infection: more than just killers [J].
Andoniou, Christopher E. ;
Andrews, Daniel M. ;
Degli-Esposti, Mariapia A. .
IMMUNOLOGICAL REVIEWS, 2006, 214 :239-250
[5]   Impaired dendritic cell maturation in patients with chronic, but not resolved, hepatitis C virus infection [J].
Auffermann-Gratzinger, S ;
Keeffe, EB ;
Levy, S .
BLOOD, 2001, 97 (10) :3171-3176
[6]   Impaired allostimulatory function of dendritic cells in chronic hepatitis C infection [J].
Bain, C ;
Fatmi, A ;
Zoulim, F ;
Zarski, JP ;
Trépo, C ;
Inchauspé, G .
GASTROENTEROLOGY, 2001, 120 (02) :512-524
[7]   A FADD-dependent innate immune mechanism in mammalian cells [J].
Balachandran, S ;
Thomas, E ;
Barber, GN .
NATURE, 2004, 432 (7015) :401-405
[8]   COMPLEX-FORMATION BETWEEN THE NS3 SERINE-TYPE PROTEINASE OF THE HEPATITIS-C VIRUS AND NS4A AND ITS IMPORTANCE FOR POLYPROTEIN MATURATION [J].
BARTENSCHLAGER, R ;
LOHMANN, V ;
WILKINSON, T ;
KOCH, JO .
JOURNAL OF VIROLOGY, 1995, 69 (12) :7519-7528
[9]   Viral recognition by Toll-like receptors [J].
Barton, Gregory M. .
SEMINARS IN IMMUNOLOGY, 2007, 19 (01) :33-40
[10]   Liver expression of proteins controlling interferon-mediated signalling as predictive factors in the response to therapy in patients with hepatitis C virus infection [J].
Bautista, D. ;
Bermudez-Silva, F. J. ;
Lasarte, J. J. ;
Rodriguez-Fonseca, F. ;
Baixeras, E. .
JOURNAL OF PATHOLOGY, 2007, 213 (03) :347-355