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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Springer seminars in immunopathology 17 (1995), S. 261-281 
    ISSN: 1432-2196
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Approximately 5% of the world population is infected by the hepatitis B virus (HBV) which causes a necroinflammatory liver disease of variable duration and severity. Chronically infected patients with active liver disease carry a high risk of developing cirrhosis and hepatocellular carcinoma. The immune response to HBV-encoded antigens is responsible both for viral clearance and for disease pathogenesis during this infection. While the humoral antibody response to viral envelope antigens contributes to the clearance of circulating virus particles, the cellular immune response to the envelope, nucleocapsid and polymerase antigens eliminates infected cells. The class I- and class II-restricted T cell responses to the virus are vigorous, polyclonal and multispecific in acutely infected patients who successfully clear the virus, and they are relatively weak and more narrowly focussed in chronically infected patients who do not. The pathogenetic and antiviral potential of the cytotoxic T lymphocyte (CTL) response to HBV have been demonstrated by the induction of a severe necroinflammatory liver disease following the adoptive transfer of HBV surface antigen-specific CTL into HBV transgenic mice, and by the noncytolytic suppression of viral gene expression and replication in the same animals by a post-transcriptional mechanism mediated by interferon-γ, tumor necrosis factor-α and interleukin-2. The dominant cause of viral persistence during HBV infection is the development of a weak antiviral immune response to the viral antigens. While neonatal tolerance probably plays an important role in viral persistence in patients infected at birth, the basis for poor responsiveness in adult onset infection is not well understood and requires further analysis. Viral evasion by epitope inactivation and T cell receptor antagonism may contribute to the worsening of viral persistence in the setting of an ineffective immune response, as can the incomplete down-regulation of viral gene expression and the infection of immunologically privileged tissues. Chronic liver cell injury and the attendant inflammatory and regenerative responses create the mutagenic and mitogenic stimuli for the development of DNA damage that can cause hepatocellular carcinoma. Elucidation of the immunological and virological basis for HBV persistence may yield immunotherapeutic and antiviral strategies to terminate chronic HBV infection and reduce the risk of its life-threatening sequellae.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Springer seminars in immunopathology 19 (1997), S. 57-68 
    ISSN: 1432-2196
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Hepatitis C virus (HCV) infection becomes persistent in the majority of instances in the face of a Immoral and cellular immune response, and persistent HCV infection is associated with chronic hepatitis. In particular, cytotoxic T lymphocytes (CTL), crucial in the eradication of virus-infected cells, have been observed in the liver and the peripheral blood of chronically infected patients, suggesting that CTL cannot completely eliminate the virus, and may contribute to chronic liver injury. In this review, the potential host and the viral factors involved in the pathogenesis of chronic HCV infection will be discussed with emphasis on the HLA-A2 restricted peripheral blood CTL response and its relationship to liver disease and viral load.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Springer seminars in immunopathology 3 (1981), S. 439-459 
    ISSN: 1432-2196
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Conclusion In conclusion, until the cellular biology of hepatitis B virus infection is understood and until the technology for the development of suitable virus infected autologous target cells is available, it will not be possible to definitively establish the mechanism involved in the pathogenesis of hepatitis B virus induced hepatocellular injury. Clearly, considerable effort must now be focused on the basic biology of virus infection, replication, and effects on hepatocellular metabolism before it will be possible to perform the definitive experiments to elucidate the role played by the immune system in the pathogenesis of this disease.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 436 (2005), S. 930-932 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] The human suffering exacted by the hepatitis C virus is enormous. Hundreds of thousands of people die each year from liver failure and cancer caused by this infection. There is no vaccine, and the available antiviral drugs are toxic, expensive and only partly effective. Progress has been hindered ...
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  • 5
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 449 (2007), S. 919-922 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] RNA interference through non-coding microRNAs (miRNAs) represents a vital component of the innate antiviral immune response in plants and invertebrate animals; however, a role for cellular miRNAs in the defence against viral infection in mammalian organisms has thus far remained elusive. Here ...
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  • 6
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 369 (1994), S. 407-410 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Residues 18-27 of the hepatitis B virus (HBV) nucleoprotein contain an HLA-A2-restricted CTL epitope9, and an efficient response against it and other epitopes derived from the viral nucleocapsid10, envelope11 and polymerase (F.V.C. et aL, manuscript in preparation) proteins is observed in ...
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  • 7
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature medicine 11 (2005), S. 1167-1169 
    ISSN: 1546-170X
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] We found that platelet depletion reduces intrahepatic accumulation of virus-specific cytotoxic T lymphocytes (CTLs) and organ damage in mouse models of acute viral hepatitis. Transfusion of normal but not activation-blocked platelets in platelet-depleted mice restored accumulation of CTLs and ...
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Springer seminars in immunopathology 12 (1990), S. 25-31 
    ISSN: 1432-2196
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Conclusions The pathogenesis of HBV-induced hepatocellular injury still remains unsolved despite several years of continuous research effort by a number of investigators. A plausible hypothesis is shown in Fig. 1. The central issue is the role of CTL in causing liver cell death and HBV clearance. Although the HBV nucleoprotein has been suggested to be a major target antigen for CTL [16], it is entirely possible that selected regions of the viral envelope and other nonstructural proteins such as the polymerase may serve as target structure for HLA class I- or class II-restricted CTL recognition, as has been shown in other viral systems. CTL might in turn be negatively modulated by antibody masking of target antigen(s) [22] and by specific intrahepatic suppressor T cells which have been recently demonstrated to be active in chronic HBV infection [4]. In addition, helper T lymphocytes may exert an indirect cytotoxic effect through the release of cytokines such as tumor necrosis factor [5]. This circuit can be potentially amplified by soluble factor(s) secreted by autoreactive cells [5]. Finally, antibody-dependent cell-mediated cytotoxicity (ADCC) may also be a determinant of liver cell necrosis as has been suggested earlier [12]. The use of molecular vectors and of synthetic peptides derived from the various viral protein sequences will help us to dissect the immune response to HBV. We anticipate that this strategy will permit us to identify the function, phenotype, HLA restriction and antigenic fine specificity of HBV-specific CTL in HBV infection with the hope that such knowledge may ultimately be translated into more specific and effective therapeutic strategies for eradication of persistent HBV infection and associated liver disease in the future.
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  • 9
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature medicine 2 (1996), S. 1104-1108 
    ISSN: 1546-170X
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] It is widely believed that the hepatitis B virus (HBV) is completely cleared by antiviral antibodies and specific cytotoxic T lymphocytes (CTLs) during acute viral hepatitis. We now demonstrate that traces of HBV are often detectable in the blood for many years after clinical recovery from acute ...
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  • 10
    Electronic Resource
    Electronic Resource
    Palo Alto, Calif. : Annual Reviews
    ISSN: 1553-4006
    Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Topics: Medicine
    Notes: Among the many viruses that are known to infect the human liver, hepatitis B virus (HBV) and hepatitis C virus (HCV) are unique because of their prodigious capacity to cause persistent infection, cirrhosis, and liver cancer. HBV and HCV are noncytopathic viruses and, thus, immunologically mediated events play an important role in the pathogenesis and outcome of these infections. The adaptive immune response mediates virtually all of the liver disease associated with viral hepatitis. However, it is becoming increasingly clear that antigen-nonspecific inflammatory cells exacerbate cytotoxic T lymphocyte (CTL)-induced immunopathology and that platelets enhance the accumulation of CTLs in the liver. Chronic hepatitis is characterized by an inefficient T cell response unable to completely clear HBV or HCV from the liver, which consequently sustains continuous cycles of low-level cell destruction. Over long periods of time, recurrent immune-mediated liver damage contributes to the development of cirrhosis and hepatocellular carcinoma.
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