Viral determinants and host immune responses in the pathogenesis of HBV infection

被引:55
作者
Rapicetta, M
Ferrari, C
Levrero, M
机构
[1] Univ Roma La Sapienza, Fdn Andrea Cesalpino, Gene Express Lab, Policlin Umberto I, I-00161 Rome, Italy
[2] Ist Super Sanita, Virol Lab, I-00161 Rome, Italy
[3] Azienda Ospedaliera Parma, Div Malattie Infett & Immunopatol Virale, Parma, Italy
[4] Univ Cagliari, Dept Internal Med, I-09124 Cagliari, Italy
关键词
HBV; infection; virus; immunity; pathogenesis;
D O I
10.1002/jmv.10096
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Hepatitis B virus (HBV) is a virus that infects about 350,000,000 people worldwide with a clinical spectrum of acute hepatitis, the healthy carrier state, cirrhosis and hepatocellular carcinoma (HCC). The outcome of HBV infection is the result of complicated viral-host interactions. As in other infections with non-cythopatic viruses, the immune response is thought to play a crucial role in disease pathogenesis but there is increasing evidence that a variety of viral mechanisms, some depending on the function of virally encoded proteins, have a profound impact on the infected hepatocytes, the liver microenvironment, and host anti-viral responses. Indeed, the virus has evolved multiple mechanisms to ensure its success in infecting a susceptible host. The essential aspects of the life cycle of HBV and the host immune response are reviewed and recent new developments in the molecular virology of HBV, including experimental animal models, in the role of accessory viral proteins in disease pathogenesis and HCC development and in the characterisation of the T cell response in the control of HBV infection, are highlighted. (C) 2002 Wiley-Liss, Inc.
引用
收藏
页码:454 / 457
页数:4
相关论文
共 21 条
[1]   Hepadnavirus evolution and molecular strategy of adaptation in a new host [J].
Argentini, C ;
La Sorsa, V ;
Bruni, R ;
D'Ugo, E ;
Giuseppetti, R ;
Rapicetta, M .
JOURNAL OF GENERAL VIROLOGY, 1999, 80 :617-626
[2]   Different cytokine profiles of intrahepatic T cells in chronic hepatitis B and hepatitis C virus infections [J].
Bertoletti, A ;
DElios, MM ;
Boni, C ;
DeCarli, M ;
Zignego, AL ;
Durazzo, M ;
Missale, G ;
Penna, A ;
Fiaccadori, F ;
DelPrete, G ;
Ferrari, C .
GASTROENTEROLOGY, 1997, 112 (01) :193-199
[3]   Lamivudine treatment can overcome cytotoxic T-cell hyporesponsiveness in chronic hepatitis B: New perspectives for immune therapy [J].
Boni, C ;
Penna, A ;
Ogg, GS ;
Bertoletti, A ;
Pilli, M ;
Cavallo, C ;
Cavalli, A ;
Urbani, S ;
Boehme, R ;
Panebianco, R ;
Fiaccadori, F ;
Ferrari, C .
HEPATOLOGY, 2001, 33 (04) :963-971
[4]  
BRECHOT C, 1997, VIRAL HEPATITIS LIVE, P490
[5]   RECURRENCE OF WHV INTEGRATION IN THE B3N LOCUS IN WOODCHUCK HEPATOCELLULAR-CARCINOMA [J].
BRUNI, R ;
ARGENTINI, C ;
DUGO, E ;
GIUSEPPETTI, R ;
CICCAGLIONE, AR ;
RAPICETTA, M .
VIROLOGY, 1995, 214 (01) :229-234
[6]   Activation of the N-myc2 oncogene by woodchuck hepatitis virus integration in the linked downstream b3n locus in woodchuck hepatocellular carcinoma [J].
Bruni, R ;
D'Ugo, E ;
Giuseppetti, R ;
Argentini, C ;
Rapicetta, M .
VIROLOGY, 1999, 257 (02) :483-490
[7]   The hepatitis B virus X gene induces p53-mediated programmed cell death [J].
Chirillo, P ;
Pagano, S ;
Natoli, G ;
Puri, PL ;
Burgio, VL ;
Balsano, C ;
Levrero, M .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (15) :8162-8167
[8]   Identification of scaffold/matrix attachment region in recurrent site of woodchuck hepatitis virus integration [J].
D'Ugo, E ;
Bruni, R ;
Argentini, C ;
Giuseppetti, R ;
Rapicetta, M .
DNA AND CELL BIOLOGY, 1998, 17 (06) :519-527
[9]  
Gottlob K, 1998, CANCER RES, V58, P3566
[10]   Viral clearance without destruction of infected cells during acute HBV infection [J].
Guidotti, LG ;
Rochford, R ;
Chung, J ;
Shapiro, M ;
Purcell, R ;
Chisari, FV .
SCIENCE, 1999, 284 (5415) :825-829