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Hepat Mon. 2015 Jun 23;15(6):e29477. doi: 10.5812/hepatmon.29477v2. eCollection 2015 Jun.

Genomic Diversity of Hepatitis B Virus Infection Associated With Fulminant Hepatitis B Development.

Author information

1
Department of Microbiology and Immunology, Laboratory of Clinical and Epidemiological Virology, Rega Institute for Medical Research, KU Leuven, Leuven, Belgium.
2
Department of Molecular Microbiology and Immunology, Harlyne J. Norris Cancer Research Tower, Keck School of Medicine, University of Southern California, Los Angeles, USA.
3
Department of Medicine III, RWTH-University Hospital Aachen, Aachen, Germany.
4
Department of Microbiology and Immunology, Laboratory of Clinical and Epidemiological Virology, Rega Institute for Medical Research, KU Leuven, Leuven, Belgium ; Blood Transfusion Research Centre, High Institute for Research and Education in Transfusion Medicine, Tehran, IR Iran.

Abstract

CONTEXT:

After five decades of Hepatitis B Virus (HBV) vaccine discovery, HBV is still a major public health problem. Due to the high genetic diversity of HBV and selective pressure of the host immune system, intra-host evolution of this virus in different clinical manifestations is a hot topic of research. HBV infection causes a range of clinical manifestations from acute to chronic infection, cirrhosis and hepatocellular carcinoma. Among all forms of HBV infection manifestations, fulminant hepatitis B infection possesses the highest fatality rate. Almost 1% of the acutely infected patients develop fulminant hepatitis B, in which the mortality rate is around 70%.

EVIDENCE ACQUISITION:

All published papers deposited in Genbank, on the topic of fulminant hepatitis were reviewed and their virological aspects were investigated. In this review, we highlight the genomic diversity of HBV reported from patients with fulminant HBV infection.

RESULTS:

The most commonly detected diversities affect regulatory motifs of HBV in the core and S region, indicating that these alterations may convert the virus to an aggressive strain. Moreover, mutations at T-cell and B-cell epitopes located in pre-S1 and pre-S2 proteins may lead to an immune evasion of the virus, likely favoring a more severe clinical course of infection. Furthermore, point and frame shift mutations in the core region increase the viral replication of HBV and help virus to evade from immune system and guarantee its persistence.

CONCLUSIONS:

Fulminant hepatitis B is associated with distinct mutational patterns of HBV, underlining that genomic diversity of the virus is an important factor determining its pathogenicity.

KEYWORDS:

Hepatitis B Virus; Human Genome Project; Liver Failure, Acute

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