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Journal of Hepatology Aug 2017
Topics: Antiviral Agents; Hepatitis B; Hepatitis B virus; Hepatitis B, Chronic; Humans
PubMed: 28629790
DOI: 10.1016/j.jhep.2017.04.015 -
Seminars in Cancer Biology Dec 2013All members of the family Hepadnaviridae are primarily viruses which contain double-stranded DNA genomes that are replicated via reverse transcription of a pregenomic... (Review)
Review
All members of the family Hepadnaviridae are primarily viruses which contain double-stranded DNA genomes that are replicated via reverse transcription of a pregenomic RNA template. There are two subgroups within this family: mammalian and avian. The avian member's include the duck hepatitis B virus (DHBV), heron hepatitis B virus, Ross goose hepatitis B virus, stork hepatitis B virus and the recently identified parrot hepatitis B virus. More recently, the detection of endogenous avian hepadnavirus DNA integrated into the genomes of zebra finches has revealed a deep evolutionary origin of hepadnaviruses that was not previously recognised, dating back over 40 million years ago. The non-primate mammalian members of the Hepadnaviridae include the woodchuck hepatitis virus (WHV), the ground squirrel hepatitis virus and arctic squirrel virus, as well as the recently described bat hepatitis virus. The identification of hepatitis B virus (HBV) in higher primates such as chimpanzee, gorilla, orangutan, and gibbons that cluster with the human genotypes further implies a more complex origin of this virus. By studying the molecular epidemiology of HBV in indigenous and relict populations in Asia-Pacific we propose a model for the origin and evolution of HBV that involves multiple cross-species transmissions and subsequent recombination events on a background of genotype C HBV infection.
Topics: Animals; Evolution, Molecular; Genotype; Hepatitis B virus; Humans; Phylogeny; Phylogeography
PubMed: 24013024
DOI: 10.1016/j.semcancer.2013.08.006 -
Antimicrobial Agents and Chemotherapy Dec 2007
Topics: Drug Resistance, Viral; Hepatitis B virus; Humans; Lamivudine; Reverse Transcriptase Inhibitors; Virus Replication
PubMed: 18025122
DOI: 10.1128/AAC.00840-07 -
Reviews in Medical Virology Jan 2009The mechanisms for HBV persistence and the pathogenesis of chronic HB have been shown mainly due to defects in host immune responses. However, HBV isolates with... (Review)
Review
The mechanisms for HBV persistence and the pathogenesis of chronic HB have been shown mainly due to defects in host immune responses. However, HBV isolates with different biological features may also contribute to different clinical outcomes and epidemiological implications in viral hepatitis B (HB). This review presents interesting biological features of HBV isolates based on the structural and functional analysis of full-length HBV isolates from various patients. Among isolates from children after failure of HB vaccination, 129L mutant at the 'a' determinant was found with normal binding efficiency to anti-HBs, but with reduced immunogenicity, which could initiate persistent HBV infections. Isolates from fulminant hepatitis (FH) B patients were not all highly replicative, but differences in capacities of anti-HBs induction could be involved in the pathogenesis of FH. The high replicative competency of isolates from hepatocellular carcinoma (HCC) patients could result in enhanced immune-mediated cytopathic effects against HBV viral proteins, and increased transactivating activity by the X protein. The mechanism of a double-spliced variant in enhancing replication of the wild-type virus is presented. The importance of integrating structural and functional analysis to reveal biological features of HBV isolates in viral pathogenesis is discussed.
Topics: Child; Genome, Viral; Hepatitis B; Hepatitis B virus; Humans; Virulence; Virus Replication
PubMed: 19058172
DOI: 10.1002/rmv.600 -
World Journal of Gastroenterology Jan 2007Hepatitis B virus (HBV) is a member of the hepadnavirus family. Hepadnaviruses can be found in both mammals (orthohepadnaviruses) and birds (avihepadnaviruses). The... (Review)
Review
Hepatitis B virus (HBV) is a member of the hepadnavirus family. Hepadnaviruses can be found in both mammals (orthohepadnaviruses) and birds (avihepadnaviruses). The genetic variability of HBV is very high. There are eight genotypes of HBV and three clades of HBV isolates from apes that appear to be additional genotypes of HBV. Most genotypes are now divided into subgenotypes with distinct virological and epidemiological properties. In addition, recombination among HBV genotypes increases the variability of HBV. This review summarises current knowledge of the epidemiology of genetic variability in hepadnaviruses and, due to rapid progress in the field, updates several recent reviews on HBV genotypes and subgenotypes.
Topics: Animals; Avihepadnavirus; DNA, Recombinant; DNA, Viral; Genotype; Hepatitis B; Hepatitis B virus; Humans; Orthohepadnavirus; Phylogeny; Prevalence
PubMed: 17206751
DOI: 10.3748/wjg.v13.i1.14 -
Antiviral Therapy 2008Hepatitis B virus (HBV) infection is a global health issue. Effective and individualized treatment of chronic hepatitis B to prevent progression to end-stage liver... (Review)
Review
Hepatitis B virus (HBV) infection is a global health issue. Effective and individualized treatment of chronic hepatitis B to prevent progression to end-stage liver diseases and hepatocellular carcinoma is needed. HBV can be classified into eight genotypes (A-H) on the basis of genome sequence divergence. In addition, several naturally occurring HBV mutants have also been identified. The epidemiology of HBV genotypes and their implications for response to antiviral therapy have become increasingly recognized. Recent studies suggested that responses to standard interferon treatment in patients with genotype A or B are better than those with genotype C or D; however, conflicting results exist regarding the response to pegylated interferon. The influence of dose and duration on interferon-based therapy remains to be clarified. In addition to genotype, naturally occurring mutations such as precore and core promoter mutations have also attracted much attention, because they have been shown to affect the disease progression of HBV-related chronic liver disease and possibly the response to antiviral therapy. Here, we review the differences in antiviral theraputic response among HBV genotypes and discuss the role of precore or core promoter mutations in response to antiviral therapy.
Topics: Antiviral Agents; Genetic Variation; Hepatitis B; Hepatitis B virus; Humans; Treatment Outcome
PubMed: 18771045
DOI: No ID Found -
Alimentary Pharmacology & Therapeutics Feb 2023
Topics: Humans; Hepatitis B virus
PubMed: 36641789
DOI: 10.1111/apt.17355 -
Medecine Sciences : M/S Nov 2022
Topics: Humans; Hepatitis B virus
PubMed: 36448889
DOI: 10.1051/medsci/2022136 -
Journal of Hepatology Aug 2021Although discontinuation of nucleos(t)ide analogue (NA) treatment before HBsAg loss is part of all current HBV treatment guidelines for HBeAg-positive patients who... (Review)
Review
Although discontinuation of nucleos(t)ide analogue (NA) treatment before HBsAg loss is part of all current HBV treatment guidelines for HBeAg-positive patients who achieve HBeAg seroconversion, a treatment endpoint known to be associated with silencing of HBV transcriptional activity and restoration of HBV-specific immune control, whether it is even appropriate to consider NA discontinuation before HBsAg loss in the HBeAg-negative phase remains highly controversial. Despite the growing evidence that a relevant, albeit small, proportion of patients with HBeAg-negative disease can be cured by stopping NA treatment, the fear of discontinuation-associated relapse and the uncertainty of how to predict off-therapy response and monitor patients after discontinuation have generated scepticism and subsequently led to low implementation of this concept in the clinic. In this article, we propose a concept in which NA discontinuation-associated relapse is an integral part of the stop-to-cure approach and ultimately the trigger for achieving HBsAg loss. However, the relapse in this sense becomes functionally effective only if HBV-specific immune reinvigoration and silencing of HBV transcriptional activity have been achieved during the NA treatment period. The probability of functional cure and the severity of post-discontinuation flares depend on the underlying baseline transcriptional activity of HBV when NA therapy was started, as well as the duration of NA treatment, both factors that should be considered as we move towards individualised approaches to HBV cure.
Topics: Hepatitis B virus; Humans; Nucleosides; Seroconversion; Treatment Outcome
PubMed: 33957187
DOI: 10.1016/j.jhep.2021.04.040 -
Antiviral Therapy 2010The emergence of hepatitis B virus (HBV) drug-resistant (and multidrug-resistant) strains during long-term therapy with nucleoside/nucleotide analogues is associated... (Review)
Review
The emergence of hepatitis B virus (HBV) drug-resistant (and multidrug-resistant) strains during long-term therapy with nucleoside/nucleotide analogues is associated with treatment failure and, therefore, represents a clinical challenge. For clinicians, the close monitoring and management of resistance has become a key issue in clinical practice. For HBV virologists, the understanding of the mechanism of emergence of specific mutant strains in the viral quasispecies during treatment is also an important issue. If a particular viral strain can emerge in the quasispecies within a particular environment, it is probably because its fitness is superior to other strains. The present review focuses on viral fitness as well as viral infectivity, and in particular on technical means that are available to study this viral fitness in vitro and in animal models.
Topics: Animals; Antiviral Agents; Biomedical Research; Disease Models, Animal; Drug Resistance, Viral; Hepatitis B; Hepatitis B virus; Humans; Mice; Mutation; Pan troglodytes; Virus Replication
PubMed: 20516574
DOI: 10.3851/IMP1551