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)

The intravenous infusion of fresh-frozen plasma is an alternative to intramuscular immune serum globulin (ISG) injections. When given in doses of 15 ml/kg at 3-week intervals, the IgG levels achieved are significantly higher than those achieved by 0.7 ml/kg of ISG and they persist longer. In addition, IgM and IgA levels are raised slightly. Other advantages of plasma include the avoidance of intramuscular infections, better patient tolerance, and provision of other serum proteins. The chief disadvantages of plasma are the risk of serum hepatitis (which can be minimized by donor selection) and the inconvenience of procurement and administration. However, it is the treatment of choice for Wiskott-Aldrich syndrome, certain opsonic deficiencies and patients refractory, sensitive or unable to have ISG injections.
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PMID:Plasma therapy: an alternative to gamma globulin injections in immunodeficiency. 80 75

Testing of paired serum samples of 12 children with the Wiskott-Aldrich syndrome for the presence of hepatitis B surface antigen (HBsAg) antibody to HB, Ag, and antibody to the hepatitis B core antigen revealed evidence of hepatitis B virus infection in three. None of the three, however, developed overt clinical hepatitis or the chronic HBsAg carrier state. These data suggest that the immunologic defects seen in the Wiskott-Aldrich syndrome permit adequate immune responses to the hepatitis B virus and do not predispose to the chronic HBsAg carrier state.
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PMID:Hepatitis B virus infection in the Wiskott-Aldrich syndrome. 125 11

We characterized a number of important features of the structure of the cohesive overlap region of the DNA genome of duck hepatitis B virus. The 5'-terminal nucleotide of minus-strand DNA was localized to nucleotide 2537, a G residue within the 12-base repeat sequence DR1. This G residue was shown to be the site of a covalent linkage to a protein, consistent with speculation that this protein is the primer of minus-strand synthesis, which occurs by reverse transcription. The 3' terminus of the minus strand was heterogeneous, being mapped to nucleotides 2530 and 2531, indicating that the minus strand is terminally redundant by seven or eight bases and ends at the putative 5' end of the transcribed RNA template (pregenome) for reverse transcription. We previously demonstrated that the presumptive RNA primer of plus-strand synthesis remains attached to plus-strand DNA during virus maturation; moreover, the sequence of this primer suggested an origin from the 5' end of the pregenome (J.-M. Lien, C. E. Aldrich, and W. S. Mason, J. Virol. 57:229-236, 1986). We show here that over 75% of plus-strand primers are capped, further supporting the idea that these primers are uniquely derived from the 5' end of the pregenome. Finally, we found that seemingly mature duck hepatitis B virus genomes are incomplete by at least 12 bases, in that the 12-base repeat sequence DR2 is not copied into plus-strand DNA during virus maturation. Since DR2 in virion DNA is duplexed with the RNA primer of plus-strand synthesis, it is possible that the failure to make complete plus strands is due to an inability of the viral DNA polymerase to carry out a displacement of the bound RNA primer.
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PMID:Initiation and termination of duck hepatitis B virus DNA synthesis during virus maturation. 368 60

Duck hepatitis B virus (DHBV) DNA synthesis in congenitally infected ducks is inhibited by 2'-deoxycarbocyclic guanosine (2'-CDG). Three months of therapy reduces the number of infected hepatocytes at least 10-fold (W.S. Mason, J. Cullen, J. Saputelli, T.-T. Wu, C. Liu, W.T. London, E. Lustbader, P. Schaffer, A.P. O'Connell, I. Fourel, C.E. Aldrich, and A.R. Jilbert, Hepatology 19:393-411, 1994). The present study was performed to determine the kinetics of disappearance of infected hepatocytes and to evaluate the role of hepatocyte turnover in this process. Essentially all hepatocytes were infected before drug therapy. Oral treatment with 2'-CDG resulted in a prompt reduction in the number of infected hepatocytes. After 2 weeks, only 30 to 50% appeared to still be infected, and less than 10% were detectably infected after 5 weeks of therapy. To assess the possible role of hepatocyte turnover in these changes, 5-bromo-2'-deoxyuridine (BUdR) was administered 8 h before liver biopsy to label host DNA in hepatocytes passing through S phase, and stained nuclei were detected in tissue sections by using an antibody reactive to BUdR. The extent of nuclear labeling after 5 weeks was the same as that before therapy (ca. 1%). However, biopsies taken after 2 weeks of therapy showed a ca. 10-fold elevation in the number of nuclei labeled with BUdR. This result suggested that a rapid clearance of infected hepatocytes by 2'-CDG was caused not just by the inhibition of viral replication but also by an acceleration of the rate of hepatocyte turnover. To test this possibility further, antiviral therapy was carried out with another strong inhibitor of DHBV DNA synthesis, 5-fluoro-2',3'-dideoxy-3'-thiacytidine (524W), which did not accelerate hepatocyte turnover in ducks. 524W administration led to a strong inhibition of virus production but to a slower rate of decline in the number of infected hepatocytes, so that ca. 50% (and perhaps more) were still infected after 3 months of therapy. In addition, histopathologic evaluation of 2'-CDG-treated ducks revealed liver injury, especially at the start of therapy. No liver damage was observed during 524W therapy. These results imply that clearance of infected hepatocytes from the liver is correlated with hepatocyte turnover. Thus, in the absence of immune clearance or other sources for the accelerated elimination of infected hepatocytes, inhibitors of virus replication would have to be administered for a long period to substantially reduce the burden of infected hepatocytes in the liver.
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PMID:Evidence that hepatocyte turnover is required for rapid clearance of duck hepatitis B virus during antiviral therapy of chronically infected ducks. 796 25

OBJECTIVE: To evaluate the prevalence of anti-HCV antibodies using subjects hospitalized in surgical departments and medical wards, and out-patients; secondly, to assess the evidence for developing chronic hepatitis in subjects positive for anti-HCV when compared with those with hepatitis B virus (HBV). METHODS: 21 888 serum samples from 18 380 subjects were investigated for anti-HCV antibodies using second and third generation immunoenzymatic assays. Some of these subjects were hospitalized patients and some were out-patients. RESULTS: THE STUDY SHOWED A 12.8% OVERALL ANTI-HCV PREVALENCE RATE WITH SIGNIFICANT DIFFERENCES BETWEEN OUT-PATIENTS (16.5%) OR SUBJECTS HOSPITALISED IN MEDICAL WARDS (16%) AND IN-PATIENTS IN SURGICAL DEPARTMENTS (7.7%). THE THIRD GROUP INCLUDED ASYMPTOMATIC SUBJECTS OVER TWENTY YEARS OLD WHOSE SERA WERE TESTED FOR ANTI-HCV ANTIBODIES AS PART OF ROUTINE PREOPERATION SCREENING AND NOT ON CLINICAL SUSPICION. HENCE, THIS GROUP, TOO, CAN BE CONSIDERED AS REPRESENTATIVE OF THE GENERAL POPULATION, AND THE PREVALENCE OF ANTI-HCV ANTIBODIES OBSERVED AMONG THEM AS THE PREVALENCE OF ANTI-HCV ANTIBODIES IN THE GENERAL POPULATION IN A NORTHERN ITALIAN AREA. THE DATA, FOLLOWING A CONFIRMATORY TEST (RIBA) ON POSITIVE SAMPLES, WERE ANALYSED FOR THEIR POSITIVITY TO DIFFERENT ANTIGENS (THE SIMULTANEOUS PRESENCE OF ANTIBODIES TO THE C-100, C-33 AND C-22 ANTIGENS), AS AN INDEX OF DEVELOPING CHRONIC VIRAL ACTIVITY. THIS WAS OBSERVED IN 63.4% OF POSITIVE PATIENTS FROM SURGICAL DEPARTMENTS: CONCLUSIONS: There is a large proportion of the asymptomatic population which could be chronically infected.
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PMID:Prevalence of hepatitis C virus antibodies in a clinic-based group of Italians from one geographic area. 1185 35