Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We identified a novel spliced RNA of 2.6 kb from a human hepatoma cell line HepG2 transfected with the hepatitis B virus (HBV) genome. The splicing acceptor site of the novel 2.6-kb RNA (position 489) was shown to be common to that of the previously described 2.1-kb spliced RNA which codes for an altered core antigen lacking the carboxy-terminal amino acid, cysteine. However, the donor site of the 2.6-kb RNA is different from any of the spliced RNA reported and located at 538 nucleotides (nt) downstream of the donor site of the 2.1-kb RNA. Introduction of single-base change mutations in the consensus sequence of the donor site of the 2.1-kb RNA maintained the splicing by using the cryptic donor site. The amount of the 2.6-kb spliced RNA was unchanged by these mutations. These results suggest independent regulations for the synthesis of the 2.1- and 2.6-kb spliced RNAs.
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PMID:Alternative splicing of hepatitis B virus RNAs in HepG2 cells transfected with the viral DNA. 223 78

The recognition of replicating hepatitis B virus (HBV) may be important to both define the cause of and know how to manage chronic liver disease in multitransfused hemophilic patients. Replicating HBV can be detected at the molecular level by methods for HBV-specific DNA (HBV-DNA), which are much more sensitive than the immunologic methods for detecting hepatitis B surface antigen (HBsAg) and hepatitis B e antigen (HBeAg). Unselected hemophilic patients (260; 6% with HBsAg, 4% with isolated anti-hepatitis B core (anti-HBc), 52% with anti-HBs and anti-HBc, 26% with isolated anti-HBs, and 12% with no HBV marker) were investigated retrospectively with a dot spot hybridization technique that detects serum HBV-DNA down to 0.5 pg and by Southern blot analysis, which tests the specificity of the HBV-DNA reactions. Eighteen patients (7%; five with serum HBsAg and 13 HBsAg seronegative with antibodies to HBV) had serum HBV-DNA. Serum HBV-DNA was detected more frequently in HBsAg carriers than in seronegative patients (33% versus 6%, P less than .01), and had no relationship to serum alanine aminotransferase. Serum HBV-DNA was more sensitive than the radioimmunoassay for HBeAg was for detecting replicating HBV (7% versus 1.1%, P less than .01). These findings demonstrate that there is cryptic HBV infection in a number of hemophiliacs and that serum HBV-DNA may coexist with markers thought to reflect immunity against HBV.
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PMID:Serum hepatitis B virus DNA detects cryptic hepatitis B virus infections in multitransfused hemophilic patients. 232 16

Hepatitis B virus (HBV) replicating in patients with serum hepatitis B surface antigen and antibody to hepatitis B e antigen (cryptic HBV replication) can be detected by a spot hybridization technique for serum HBV-DNA and by immunoperoxidase staining of hepatitis B core antigen in the liver. These methods allowed us to study the effects of chronic (13 to 82, mean 30 months) administration of low doses (10 or 15 mg/day) of prednisone to 17 patients with chronic active hepatitis and cryptic HBV replication. Liver biopsies performed before treatment demonstrated that 1 to 50% (mean 12%) of the liver cells were infected. After therapy, infected cells had disappeared in 5 (29%), were considerably reduced in 9 (53%) and remained unchanged in 3 (18%) patients. The mean percentage of infected cells in the liver biopsies performed at the end of the follow-up was 3.2 +/- 5.5% (p less than 0.005). Serum HBV-DNA was present in 12 of 13 and in 5 of 12 patients investigated before treatment and at the end of the study, respectively. Five patients harboring HBV in the liver developed cirrhosis during treatment. Our data indicate that, despite steroid therapy, HBV replication either ceased or was decreased in two thirds of the patients, while in no case it flared-up. The rise of cirrhosis was not prevented by this type of therapy.
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PMID:Cryptic hepatitis B virus replication during prednisone therapy in type B chronic active hepatitis. 367 95

A new hepatitis B vaccine has been developed which contains both HBsAg and HBeAg since evidence suggests that anti-HBe may have useful biologic activities. It was thus important to determine whether HBeAg is immunogenic in this type of a preparation. We now report data indicating that highly purified HBsAg particles, derived from HBeAg containing plasma, release a proportion of their contained cryptic HBeAg following the detergent treatment used in the preparation of this vaccine. Both the soluble and the residual particle associated HBeAg are immunogenic in guinea pigs. There was no detectable anti-HBe response in animals injected with similar HBsAg particles which had not been exposed to detergent.
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PMID:Immunogenicity of HBeAg in the New York Blood Center hepatitis B vaccine. 622 61

Antigens corresponding to infectious agents may be present in biological specimens only in a cryptic form bound to antibodies and thus may elude detection. We describe a solid-phase technique for separation of antigens from antibodies. Immune complexes are precipitated from serum by polyethylene glycol, dissociated with NaSCN and adsorbed onto nitrocellulose or polystyrene supports. Antigens remain topographically separated from antibodies after removal of NaSCN and can be detected with radiolabeled antibodies. Genomes from viruses immobilized on nitrocellulose can be identified by nucleic acid hybridization. Nanogram quantities of sequestered hepatitis B surface and core antigens and picogram amounts of hepatitis B virus DNA are detected.
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PMID:Radioimmunoassays of hidden viral antigens. 665 86

Antigens corresponding to infectious agents may be present in biological specimens only in a cryptic form bound to antibodies and, thus, may elude detection. We describe a solid phase technique for separation of antigens from antibodies. Immune complexes are precipitated from serum by polyethylene glycol, dissociated with NaSCN, and adsorbed onto nitrocellulose or polystyrene supports. Antigens remain topographically separated from antibodies after removal of NaSCN and can be detected with radiolabeled antibodies. Genomes from viruses immobilized on nitrocellulose can be identified by nucleic acid hybridization. Nanogram quantities of sequestered hepatitis B surface and core antigens and picogram amounts of hepatitis B virus DNA were detected. Antibody-bond adenovirus, herpesvirus, and measles virus antigens were discerned by the procedure.
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PMID:Radioimmunoassays of hidden viral antigens. 695 71

Core particles of hepatitis B virus are assembled from dimers of a single 185-residue (subtype adw) viral capsid or core protein (p21.5) which possesses two distinct domains: residues 1 to 144 form a minimal capsid assembly domain, and the arginine-rich, carboxyl-terminal residues 150 to 185 form a protamine-like domain that mediates nucleic acid binding. Little is known about the topography of the p21.5 polypeptide within either the p21.5 capsids or dimers. Here, using site-specific proteases and monoclonal antibodies, we have defined the accessibility of p21.5 residues in dimers and capsids assembled from wild-type and mutant hepatitis B virus core proteins in Xenopus oocytes and in vitro. The data reveal the protamine region to be accessible to external reagents in p21.5 dimers but largely cryptic in wild-type capsids. Strikingly, in capsids the only protease target region was a 9-residue peptide covering p21.5 residues Glu-145 to Asp-153, which falls largely between the two core protein domains. By analogy with protease-sensitive interdomain regions in other proteins, we propose that this peptide constitutes a hinge between the assembly and nucleic acid binding domains of p21.5. We further found that deletion or replacement of the terminal Cys-185 residue greatly increased surface exposure of the protamine tails in capsids, suggesting that a known disulfide linkage involving this residue tethers the protamine region inside the core particles. We propose that disruption of this disulfide linkage allows the protamine region to appear transiently on the surface of the core particle.
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PMID:A protease-sensitive hinge linking the two domains of the hepatitis B virus core protein is exposed on the viral capsid surface. 752 91

Sporadic non-A, non-B hepatitis is the most common indication for liver transplantation in patients presenting with fulminant and subacute liver failure. This study used serological, histological, and molecular biological techniques to examine specimens from 23 consecutive patients transplanted for sporadic non-A, non-B hepatitis. No evidence was found of hepatitis C virus, hepatitis E virus, or 'cryptic' hepatitis B virus infection.
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PMID:Failure to incriminate hepatitis B, hepatitis C, and hepatitis E viruses in the aetiology of fulminant non-A non-B hepatitis. 769 4

Non-A, non-B hepatitis viruses have been implicated as the etiological agent(s) in up to 60% of patients with fulminant hepatitis. These agents are reported to induce a higher mortality than other causes of fulminant hepatitis. Hepatitis E virus (HEV) and hepatitis C virus (HCV) at present constitute the major identifiable non-A, non-B hepatitis agents. Of these, HEV has been established as the sole cause of epidemic hepatitis in Afro-Asian countries, and fulminant hepatitis has been recorded during such epidemics. However, in sporadic cases, the etiological role of HEV in fulminant hepatitis has remained uncertain. The role of HCV in acute liver disease and fulminant hepatitis remains unclear. The present study was undertaken to investigate the association of HEV and HCV in patients with fulminant hepatitis by direct detection of the viral genome using reverse transcription-polymerase chain reaction (RT-PCR). Serum samples from 50 serologically identified non-A, non-B fulminant hepatitis cases negative for cryptic hepatitis B virus (HBV) infection examined via PCR were tested for HEV and HCV RNA using RT-PCR. For HEV primers from the nonstructural region (ORF-1) were used, and for HCV primers from the highly conserved 5' untranslated regions were used. The products were analysed using agarose gel electrophoresis and confirmed by hybridisation with radiolabelled internal oligonucleotide probes. HEV was detected in 31 (62%) of the 50 fulminant non-A, non-B hepatitis cases. In 18 (36%) cases, HCV RNA was detected. In 11 (22%) of the HCV cases, the HEV genome was also amplified. In 20 (40%) cases, HEV was detected alone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Etiological role of hepatitis E virus in sporadic fulminant hepatitis. 815 8

Replication of the hepadnavirus genome occurs by reverse transcription of an RNA pregenome and is mediated by the viral polymerase; the polymerase is also required for packaging of the pregenome through interaction with the RNA packaging signal, epsilon. Previous work suggested that reverse transcription of minus-strand DNA initiates within the sequence element DR1 (direct repeat 1) and that disruption of DR1 activates a cryptic initiation site in a downstream copy of epsilon. However, using active duck hepatitis B virus polymerase expressed in a yeast Ty vector system, we demonstrate that synthesis of minus-strand DNAs with 5' ends at DR1 requires the stem-loop of epsilon, whereas the production of DNAs mapping to epsilon does not require DR1. Mutations at epsilon that remove homology between epsilon and DR1 eliminate reverse transcripts with 5' ends in DR1, and restoring homology at DR1 to a mutant epsilon partially restores DNAs mapping to DR1. Insertions of one nucleotide into the bulge region of the epsilon stem-loop increase the length of minus-strand DNA whose 5' ends map to DR1 by one nucleotide. Thus, very short minus-strand primers are initiated within epsilon, rather than in DR1 as previously supposed; they are then transferred to a four-nucleotide homology in DR1. Transfer was also observed in vivo during replication of duck hepatitis B virus in avian cells; in this case, transfer is from the 5' copy of epsilon to the 3' copy of DR1. This minus-strand transfer reaction is likely to be a general feature of all hepadnaviruses.
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PMID:Hepadnavirus reverse transcription initiates within the stem-loop of the RNA packaging signal and employs a novel strand transfer. 818 92


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