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Statements from the Taormina expert meeting on occult hepatitis B virus infection.
Giovanni Raimondo*, Jean-Pierre Allain, Maurizia R. Brunetto, Marie-Annick Buendia, Ding-Shinn Chen, Massimo Colombo, Antonio Craxi, Francesco Donato, Carlo Ferrari, Giovanni B. Gaeta, Wolfram H.Expand
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Occult hepatitis B virus infection in patients with chronic hepatitis C liver disease.
BACKGROUND Hepatitis B virus (HBV) infections in patients who lack detectable hepatitis B surface antigen (HBsAg) are called occult infections. Although such infections have been identified inExpand
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Occult hepatitis B virus infection.
The persistence of hepatitis B virus (HBV) genomes in HBV surface antigen (HBsAg) negative individuals is termed occult HBV infection. Occult HBV status is associated in some cases with mutantExpand
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Nuclear HBx binds the HBV minichromosome and modifies the epigenetic regulation of cccDNA function
HBV cccDNA, the template for transcription of all viral mRNAs, accumulates in the nucleus of infected cells as a stable episome organized into minichromosomes by histones and non-histone viral andExpand
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Hepatitis B virus maintains its pro-oncogenic properties in the case of occult HBV infection.
BACKGROUND AND AIMS Occult hepatitis B virus (HBV) infection is characterized by persistence of HBV DNA into the tissue of hepatitis B surface antigen-negative individuals. The clinical relevance ofExpand
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Hepatitis B virus replication is regulated by the acetylation status of hepatitis B virus cccDNA-bound H3 and H4 histones.
BACKGROUND & AIMS HBV covalently closed circular DNA (cccDNA), the replicative intermediate responsible for persistent HBV infection of hepatocytes, is the template for transcription of all viralExpand
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Occult HBV infection
The long-lasting persistence of hepatitis B virus (HBV) genomes in the liver (with detectable or undetectable HBV DNA in the serum) of individuals testing negative for the HBV surface antigen (HBsAg)Expand
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Hepatitis B virus PreS/S gene variants: pathobiology and clinical implications.
The emergence and takeover of hepatitis B virus (HBV) variants carrying mutation(s) in the preS/S genomic region is a fairly frequent event that may occur spontaneously or may be the consequence ofExpand
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Control of cccDNA function in hepatitis B virus infection.
The template of hepatitis B virus (HBV) transcription, the covalently closed circular DNA (cccDNA), plays a key role in the life cycle of the virus and permits the persistence of infection. NovelExpand
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IFN-α inhibits HBV transcription and replication in cell culture and in humanized mice by targeting the epigenetic regulation of the nuclear cccDNA minichromosome.
HBV infection remains a leading cause of death worldwide. IFN-α inhibits viral replication in vitro and in vivo, and pegylated IFN-α is a commonly administered treatment for individuals infected withExpand
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