Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sera from 71 patients with acute liver injury have been tested for antibodies to hepatocyte membrane lipoprotein complex (LSP) using a sensitive radioimmunoassay. Two main patterns of anti-LSP response were seen. In the first, seen in patients with type A and B viral hepatitis, anti-LSP antibodies were detectable at presentation, with the highest titres two to 10 days before the peak in serum aminotransferases and, in the hepatitis B patients, when viral DNA polymerase concentrations were still high, indicating active viral replication. These findings are consistent with the anti-LSP response being consequent on an interaction between T cells and neoantigens on the liver cell surface. A similar pattern was found in halothane hepatitis where immune responses to a halothane-altered liver membrane antigen are present early in the course of the disease. In the second type of response, exemplified by cases with paracetamol-induced hepatic necrosis, anti-LSP was only occasionally detectable at presentation, although present in very low titre later in the clinical course. This may be due to the release of altered antigen at the time of hepatocellular injury. The same pattern was found in a selected group of patients with uncomplicated acute alcoholic hepatitis, suggesting that in both these groups of patients the liver damage may have been due to a direct toxic effect on liver cells.
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PMID:Anti-LSP antibodies in acute liver disease. 708 6

The recently described protein kinase activity in hepatitis B virus core antigen particles (Albin and Robinson, J. Virol. 34:297-302, 1980) has been demonstrated here in the liver-derived core particles of ground squirrel hepatitis virus. Both protein kinase activities were initially associated with DNA polymerase-positive heavy core particles in CsCl density equilibrium gradients and shifted to polymerase-negative cores during the course of purification. The major core-associated polypeptide of each virus was the dominant species labeled. A variable number of other polypeptide species were also labeled by this reaction. Tryptic peptide mapping of both major and minor phosphorylated polypeptides of each virus resulted in similar patterns, suggesting that many of the sites of phosphorylation were the same in the components of each core particle. Hydrolysis of these phosphorylated core particles revealed a major phosphoamino acid as serine and a minor phosphoamino acid as threonine. The products of the protein kinase reaction in both human hepatitis B and ground squirrel hepatitis virus core particles, then, share many characteristics. The possible function(s) of this protein kinase activity is discussed in the light of similarly characterized activities in other animal viruses.
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PMID:Core particles of hepatitis B virus and ground squirrel hepatitis virus. II. Characterization of the protein kinase reaction associated with ground squirrel hepatitis virus and hepatitis B virus. 710 41

A DNA polymerase present in particles with a density greater than 1.20 g/cm3 and capable of using a synthetic RNA template has been sought in human malignancies. This report deals with a study of a great number of peripheral-blood samples from normal controls and patients with malignant and non-neoplastic haematological disorders. For screening purposes a simplified detection test was used. In 63 controls low levels of enzyme activity were found. The enzyme activities showed a biphasic distribution pattern. Three out of 53 patients with non-neoplastic, miscellaneous haematological disorders had an elevated enzyme level associated with active viral infections (hepatitis, mononucleosis infectiosa). In 128 patients suffering from haematological malignancies 18 out of 21 cases of elevated enzyme level were associated with the presence of more than 10% pathological cells in the white blood cell fraction.
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PMID:Particle-bound DNA polymerase activity in haematological disorders and normal controls. 713 Feb 42

Twenty-five patients with chronic type B hepatitis documented by liver biopsy were followed for 1 to 6 years with serial measurements of aminotransferase levels, hepatitis B surface antigen (HBsAg), hepatitis B e antigen (HBeAg) and antibody (anti-HBe), and hepatitis B virus DNA polymerase. Initially, all were positive for HBsAg and HBeAg and had elevations in serum aminotransferases. In follow-up, only one lost HBsAg reactivity. In 13, however, elevated aminotransferase levels spontaneously fell to normal and have remained normal. These 13 also had a seroconversion from HBeAg to anti-HBe, and all became negative for serum DNA polymerase. Most had a fall in HBsAg titer. This seroconversion occurred concurrently with or several months before the fall in aminotransferase levels. In contrast, the 12 persons who remained HBeAg positive continued to have elevated aminotransferase levels. All 10 of these patients who were initially positive for DNA polymerase remained positive. These data suggest that many patients with chronic type B hepatitis eventually have a spontaneous remission in clinical and biochemical evidence of active disease, usually heralded or accompanied by the disappearance of HBeAg and DNA polymerase.
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PMID:Seroconversion from hepatitis B e antigen to antibody in chronic type B hepatitis. 723 15

Hepatitis-B core antigen (HBcAg) was released from Dane particles previously separated from anti-HBc by repeated pelleting through sucrose gradients separated into three HBcAg populations when analysed by cesium chloride density gradient centrifugation. Heavy HBcAg particles banded at a density of 1.355 gm/ml, intermediate HBcAg particles at a density of 1.33 gm/ml, and light mediate HBcAg particles at a density of 1.30 gm/ml. Like heavy HBcAg particles, intermediate HBcAg particles contained DNA polymerase activity, but the ratio of HBcAg to DNA polymerase activity was significantly different in both populations. Intermediate HBcAg particles could not be separated from heavy HBcAg particles by rate sedimentation centrifugation. The size of the HBV-DNA and the size of its single-stranded gaps were not significantly different in heavy and intermediate HBcAg populations. Data accumulated in this paper suggest that the intermediate HBcAg particle differs from the heavy HBcAg particle by the amount of HBcAg polypeptides and the number of HBcAg determinants exhibited.
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PMID:Demonstration and partial characterization of an intermediate HBcAG (Dane particle) population. 728 14

Nine patients with chronic HBsAg-positive hepatitis and persistence of HBeAg and/or core-associated DNA polymerase activity in serum for at least 1 year were followed up regularly with liver function tests for 2--7 years after onset of illness. HBsAg was present in all patients during an average follow-up period of 5 years. Seven of the 9 patients had persistently abnormal liver function tests. Persistence of HBeAg and/or Dane particle associated DNA polymerase in serum for more than 1 year after onset of illness thus seems to indicate a further long period of HBsAg present in serum and impaired liver function.
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PMID:Long-term follow-up of chronic hepatitis patients with HBsAg, HBeAg and Dane particles associated DNA polymerase in serum. 737 28

The Dane particle is-because of its characteristics--believed to be the complete hepatitis-B-virus. Sera containing high numbers of Dane particles were shown to be highly infectious. In the present study we related the HBeAg-, the HBsAg- and the anti-HBc titer to the level of DNA polymerase activity measured in 20 fold Dane particle concentrates. The data obtained indicate that the HBeAg concentration gives a semiquantitative estimate on the number of circulating Dane particles. Mean DNA polymerase activity was found to increase with HBsAg concentration and is therefore also of value-if determined in a HBeAg positive serum- for quantitation of Dane particles. The anti-HBc titer was found to be unrelated to the number of circulating Dane particles.
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PMID:Comparison of indicators for dane particles. 739 42

A virus found in the sera of Pekin ducks appears to be a new member of the human hepatitis B-like family of viruses. This virus had a diameter of 40 nm and an appearance in the electron microscope similar to that of human hepatitis B virus. The DNA genome of the virus was circular and partially single stranded, and an endogenous DNA polymerase associated with the virus was capable of converting the genome to a double-stranded circle with a size of ca. 3,000 base pairs. An analysis for viral DNA in the organs of infected birds indicated preferential localization in the liver, implicating this organ as the site of virus replication. In all of these aspects, the virus bears a striking resemblance to human hepatitis B virus and appears to be a new member of this family, which also includes ground squirrel hepatitis virus and woodchuck hepatitis virus.
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PMID:Virus of Pekin ducks with structural and biological relatedness to human hepatitis B virus. 746 57

Enzyme-linked immunosorbent assays for detecting antibodies against hepatitis C virus and the polymerase chain reaction were tested in 82 chronic hepatitis B surface antigen carriers for their accuracy in diagnosing patients coinfected with hepatitis B and C viruses. To clarify the role of each virus in chronic hepatitis, serologic assays against hepatitis B virus were also tested. Thirteen (14.9%), 14 (17.1%) and 15 (18.3%) patients were anti-HCV positive using C100 (HCV1), JCC, and a second generation test (HCV2), respectively. HCV RNA was detected by polymerase chain reaction in 9 of 18 anti-HCV-positive cases. Although HCV1 assays were not sufficient, either the JCC or HCV2 assay detected all polymerase chain reaction-positive cases. Fifteen of 18 specimens that were positive in at least one of the three ELISA were seronegative for the hepatitis B e antigen. As judged by HBV DNA polymerase activity, titers of hepatitis B surface antigen and immunoglobulin A antibody against hepatitis B core antigen (IgA anti-HBc), activity of hepatitis B virus replication and immune response against hepatitis B virus in patients with coinfection was decreased to the level of hepatitis B virus asymptomatic carriers. These results show that hepatitis C virus appears to be the primary cause of active hepatitis in most patients with hepatitis B and hepatitis C virus coinfection.
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PMID:Coinfection of hepatitis C virus in patients with chronic hepatitis B infection. 752 35

Replication of the hepadnavirus DNA genome is accomplished via reverse transcription of an intermediate, pregenomic RNA molecule. This process is likely to be carried out by a virally encoded, multifunctional polymerase which possesses DNA- and RNA-dependent DNA polymerase and RNase H activities. However, the nature of the product(s) of the polymerase gene predicted to mediate these functions is unclear. Biochemical studies of the polymerase protein(s) have been limited by its apparent low abundance in virus particles and, until recently, the inability to express active polymerase protein(s) heterologously. We have used activity gel assays to detect DNA- and RNA-dependent DNA polymerase activities associated with highly purified duck hepatitis B virus (DHBV) core particles (S. M. Oberhaus and J. E. Newbold, J. Virol. 67:6558-6566, 1993). Now we report that the same approach identifies a 35-kDa RNase H activity in association with highly purified DHBV core particles and crude preparations of virions from DHBV-infected ducks and woodchuck hepatitis virus-infected woodchucks. This is the first report of the detection of an hepadnavirus-associated RNase H activity. Its apparent size is smaller than any of the DNA polymerase activities that we detected previously and significantly smaller than the full-length protein predicted from the polymerase open reading frame (p85 for DHBV). These data suggest that the viral polymerase and RNase H activities are separable and that these enzymes may coordinate their activities in vivo by forming a complex.
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PMID:Detection of an RNase H activity associated with hepadnaviruses. 754 85


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