Abstract
AbstractHepatitis B virus (HBV), a small DNA virus with a unique replication mode, can cause chronic hepatitis (CHB), which is characterized by the persistence of the viral covalently closed circular DNA that serves as the template for HBV replication and the production of large amounts of secreted HBV surface antigen (HBsAg) that is present in excess of the levels of infectious virus. Despite the success of currently approved antiviral treatments for CHB patients, including interferon and nucleotide analogs, which suppress HBV replication and reduce the risk of CHB-related liver diseases, these therapies fail to eradicate the virus in most of the patients. With the development of the cell and animal models for HBV study, a better understanding of the HBV life cycle has been achieved and a series of novel antiviral strategies that target different stages of HBV replication have been designed to overcome the viral factors that contribute to HBV persistence. Such basic HBV research advancements and therapeutic developments are the subject of this review.
Highlights
Hepatitis B virus (HBV) vaccines have been used widely for prevention, HBV infection remains a major health problem worldwide, with an estimated 350 million chronically infected individuals, many of whom will eventually develop severe liver diseases, including liver cirrhosis, and hepatocellular carcinoma (HCC)
Hepatitis B virus (HBV), a small DNA virus with a unique replication mode, can cause chronic hepatitis (CHB), which is characterized by the persistence of the viral covalently closed circular DNA that serves as the template for HBV replication and the production of large amounts of secreted HBV surface antigen (HBsAg) that is present in excess of the levels of infectious virus
nucleot(s)ide analogs (NAs) effectively suppress HBV replication to undetectable levels by inhibiting the viral polymerase (Pol), but rarely induce seroconversion of the HBV surface antigen (HBsAg), and viremia rebound always occurs after termination of drug treatments
Summary
Hepatitis B virus (HBV) vaccines have been used widely for prevention, HBV infection remains a major health problem worldwide, with an estimated 350 million chronically infected individuals, many of whom will eventually develop severe liver diseases, including liver cirrhosis, and hepatocellular carcinoma (HCC). The replicative cycle of HBV progresses through several well-defined steps including the binding and entry of the virus, cytosolic transport and uncoating of the nucleocapsid, formation of cccDNA in the nucleus, the transcription and translation of virus-specific genes, assembly of capsids and initiation of reverse transcription, followed by budding and secretion of virions and subviral particles (SVPs) This cycle is a sophisticated process that is tightly regulated by both host and viral factors. Higher levels of HBV expression, and particles from supernatant is infectious for primary tupaia hepatocytes; responsive to HBV inhibitors A highly flexible system for studying HBV replication and pathogenesis at the molecular level Understanding virus–host interaction of HBV infection; determining pathogenicity of mutant viruses; studying the role of viral protein in regulating the virus life cycle and in transferring hepadnavirus genomes across the species barrier Study for regulation of HBV minichromosome; sensitive ampliffication and simpliffied functional analysis of full-length HBV genomes A model system in vitro and in vivo for evaluating antiviral treatments against HBV cccDNA. Studying HBV biology and the virus’ interaction with host hepatocyte genetics and physiology
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