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- W1700156486 abstract "H epatitis B virus (HBV) has a partially douhlestranded DNA genome. It replicates via an intermediate RNA stage; it is able to do this because a reverse transcriptase, a translation product of the polymerase open reading frame (ORF) of HBV (P gene), is associated with the virion. Reverse transcriptase has poor proofreading ability, resulting in a high rate of nucleotide misincorporation during transcription. In this way, mutants are introduced into the viral pool. It is estimated that at a single nucleotide position of HBV, l-3 X 10m5 mutations occur in an infected individual each year.’ A proportion of these will survive, but only if they confer some advantage over pre-existing strains. The genome of HBV, which is 3.2 kb long, is highly compact; all of the DNA encodes proteins, some areas more than one, and the regulatory elements are found within the protein-coding regions.’ From this observation, one could surmise that HBV is so highly evolved that few of the mutations that occur during the normal replication cycle would be selected. In fact, patients with chronic hepatitis have a number of different sequences cocirculating,3 and there are regions of the genome that are not particularly conserved between isolates. On the other hand, certain small stretches of nucleotides have up to 86% homology.* However, it is possible that the virus evolves during infection within an individual only to be back-selected upon infection of a contact. Apart from the P gene, there are three other definite ORFs, those encoding the surface proteins (preSl, pre-S2, and S), the core proteins (pre-C/C and C), and the transactivating X protein, HBx (the X gene). More than one polypeptide is translated from both the S and the pre-C/C regions: in each, there are a number of in-frame initiation codons (AUG) and a single, common translational stop codon (UAG or UAA), as shown in Figures 1 and 2. The S gene has three AUG, one at the beginning of each of pre-Sl, pre-S2, and S. Thus, three proteins of 409 (128 + 55 + 226), 281(55 + 226), and 226 amino acids can be produced. Hepatitis B surface antigen (HBsAg) constitutes the common carboxyl terminus, being translated from the last AUG. The core gene has a similar arrangement to the surface gene. If initiation is at the pre-C AUG, a translational product of 212 (29 + 183) amino acids is synthesized; if it begins at the C AUG, a shorter polypeptide of 183 amino acids is produced. The latter is the major nucleocapsid protein or core antigen (HBcAg), and the former is the precursor to hepatitis B e antigen (HBeAg), a protein found free in the serum but not as an integral part of the virion (Figure 1). The 212-amino acid translational product of the pre-C/C ORF contains a signal peptide of 19 amino acids at the amino terminus.4 After the RNA-ribosomal complex binds to a receptor on the endoplasmic reticulum, the growing polypeptide is secreted into the lumen of the membrane system, where it is further modified by proteolysis of the protaminelike, nucleophilic carboxyl end. The resulting protein, HBeAg, is secreted. HBeAg has been detected on the surface of cells both as a result of vaccinia transfection studies5 and by both light and electron microscopy of hepatocytes in biopsy material.6 It is thus a possible target for the humoral immune response. The pathogenesis of HBV disease is unclear, but is widely believed to be immune in nature: cytotoxic T cells and natural killer cells are seen in large quantities in the liver during acute hepatitis.’ The most likely target molecules of this process are HBcAg and/or HBeAg’; there is little evidence that HBsAg plays a role. Antibody may be involved in viral clearance, because levels of serum complement decline rapidly during hepatitis. However, antibody-dependent cell-mediated cytotoxicity (ADCC) has not been shown to play a role in the clearance of any human virus in vivo. Evidence for a direct cytopathic effect of HBV during natural infection is lacking, but recent studies with transgenic mice reveal that both HBsAgg and HBx’O may play a role in the cellular damage that is proposed to lead eventually to hepatocellular carcinoma. A definite function for HBeAg has still to be assigned. It has been proposed to be a tolerogen, particularly in infants,” and to divert the immune effector cells away from infected hepatocytes.” HBcAg and HBeAg share humoral and T-cell (helper and per-" @default.
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- W1700156486 date "1992-02-01" @default.
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- W1700156486 title "Genetic variation in hepatitis B virus" @default.
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- W1700156486 doi "https://doi.org/10.1016/0016-5085(92)90125-i" @default.
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