Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.7.7.7 (DNA polymerase)
17,007 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Natural interferon-gamma at a dose of 0.5 x 10(6) or 1 x 10(6) IU daily was intramuscularly administered daily for 4 weeks to 15 patients with chronic hepatitis B. The efficacy and safety of the treatment were evaluated for 24 weeks following the completion of the 4-week treatment period. Persistent disappearance of HBeAg was observed in 5 of 15 patients. Serum hepatitis B virus (HBV)-related DNA polymerase disappeared in 5 of 13 patients at the end of interferon therapy. On the other hand, serum ALT and beta 2-microglobulin levels showed a significant increase during the interferon therapy period. The side effects were completely reversible. These findings suggest that interferon-gamma has an antiviral effect in patients with chronic hepatitis B and that the main mechanism of the therapeutic effect may be associated with the elimination of HBV-infected hepatocytes due to the immunopotentiating effect of the substance.
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PMID:Clinical evaluation of intramuscular administration of natural interferon-gamma in the treatment of chronic hepatitis B. 759 91

The proliferative activity and ultrastructural characteristics of proliferating biliary epithelial cells were analysed immunohistocytochemically in 39 biopsied liver specimens from patients with acute viral hepatitis, chronic hepatitis and liver cirrhosis using a monoclonal antibody against DNA polymerase alpha (DNA-PA). In acute viral hepatitis with perivenular confluent necrosis, proliferation of typical bile ducts was found frequently in portal areas. In chronic aggressive hepatitis and cirrhosis, ductular proliferation of both typical and atypical forms was found in enlarged portal and periportal areas and in confluent necrotic areas. The number of proliferating biliary epithelial cells that stained positive for DNA-PA was small. There were very few positively stained cells in atypical bile ducts in confluent necrotic areas of cirrhosis. Atypical bile ducts seen in chronic aggressive hepatitis, cirrhosis and acute hepatitis with confluent necrosis were positively stained for both cytokeratins 8 and 19. In cirrhosis, the number of stained biliary epithelial cells in typical bile ducts was larger than the number of such cells in atypical bile ducts (P < 0.01). By electron microscopy, the cells positively stained for DNA-PA were mostly so-called clear cells with irregular nuclei containing coarse nucleoplasm, and a few small cells with scanty cytoplasm and few organelles.
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PMID:Analysis of proliferating biliary epithelial cells in human liver disease using a monoclonal antibody against DNA polymerase alpha. 768 20

There are several published case series of acute hepatitis A, with coverage ranging from epidemics to case reports, that provide information regarding the clinical course and outcome of hepatitis A in patients with underlying chronic hepatitis B virus (HBV) infection (1-12). Only a few reports have addressed the outcome of hepatitis A in patients with other chronic liver diseases (2, 13). Some, but not all, of these reports suggest that hepatitis A superimposed on chronic hepatitis B or other chronic liver diseases is associated with higher peak laboratory abnormalities, more severe disease, including fulminant hepatic failure, and a higher case fatality rate. In addition, analysis of HBsAg titer and serum markers of HBV replication, including HBeAg, HBV DNA, and DNA polymerase, reveals suppression of HBV replication. With the availability of hepatitis A virus (HAV) vaccine in many countries and its imminent approval for use in the United States, the issue of whether or not patients with chronic liver diseases, including chronic HBV infection, should be a target group for vaccination to prevent hepatitis A warrants consideration. The purpose of this review is to analyze the published literature addressing the clinical course and outcome of acute hepatitis A in patients with chronic HBV infection and other chronic liver diseases to determine if hepatitis A is more severe in these patients.
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PMID:Is hepatitis A more severe in patients with chronic hepatitis B and other chronic liver diseases? 784 85

Of 798 hepatitis B virus (HBV) carriers, 22 had low titers (lower than 80% inhibition in 200- or 400-fold diluted serum) of antibody to hepatitis B core antigen (anti-HBc). Among these 22 patients, there were 12 (1.50%) with viremia who were positive for hepatitis B e antigen and had a high titer of HBV-associated DNA polymerase activity. Among these 12 patients, four showed no significant change in the anti-HBc titer, while four others showed significant increases in the anti-HBc titer during the follow-up periods. The former all remained asymptomatic carriers (ASCs), while the latter all developed chronic hepatitis (CH). The liver histology of four patients (ASC: 2, CH: 2) showed mild inflammation, and the localization of hepatitis B core antigen (HBcAg) in the liver specimens showed a nuclear pattern in the two ASCs, but a nuclear plus cytoplasmic pattern in the two CH cases. In HBV carriers, the increase in anti-HBc titer seems to be closely correlated to the change in HBcAg localization from the nucleus to the cytoplasm in the liver. Therefore, rising titers of anti-HBc were assumed to be associated with increased expression of HBcAg on the hepatocyte, and hence increased immune-mediated hepatic damage and the onset of hepatitis in ASC with low titer of anti-HBc.
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PMID:Hepatitis B virus carrier with low titer of antibody to hepatitis B core antigen. 795 45

Serum and urinary neopterin levels and serum 2',5'-oligoadenylate synthetase and DNA polymerase activities were measured in 14 patients with HBeAg-positive chronic hepatitis B treated with interferon. Treatment with interferon brought about a threefold increase over basal levels in serum and urinary neopterin levels one week after the start of treatment. Both neopterin levels remained significantly elevated during treatment but rapidly returned to basal levels after the completion of treatment. Serum and urinary neopterin levels changed with a pattern similar to that of serum 2',5'-oligoadenylate synthetase activity and with a mirror image to serum DNA polymerase activity. It is indicated that measurement of serum and urinary neopterin can be used as a marker for cell-mediated immunity during interferon therapy for chronic hepatitis B, but can not be used to predict the short-term clinical effects of interferon treatment as in the case of serum 2',5'-oligoadenylate synthetase.
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PMID:Serum and urinary neopterin levels in patients with chronic active hepatitis B treated with interferon. 800 80

The expression of intercellular adhesion molecule-1 (ICAM-1) on the hepatocyte membrane was studied in 27 patients with chronic hepatitis B and C (CHB, CHC) by immunostaining using a monoclonal antibody. ICAM-1 was expressed focally in a honeycomb-like pattern by hepatocytes in livers of 26/27 patients. The degree of ICAM-1 expression was closely related to the ALT level and the histological grade of liver damage. Abundant cytotoxic T cells (CD8+, CD11b-) were found in ICAM-1-positive areas of the liver. Zones of focal necrosis contained both ICAM-1-positive hepatocytes and cytotoxic T cells. The expression of ICAM-1 was decreased in 4/6 CHB patients after interferon-alpha therapy. No relationship between the degree of hepatocyte ICAM-1 expression and viral replication markers (DNA polymerase activity and the presence of HBcA in the liver) was observed in patients with CHB. In addition, no positive correlation was found between the distribution of ICAM-1-positive hepatocytes and HBcAg-positive hepatocytes. These results suggest that ICAM-1 may play an important role in the pathogenesis of hepatocellular injury mediated by cytotoxic T cells in CHB and CHC.
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PMID:Intercellular adhesion molecule-1 expression on the hepatocyte membrane of patients with chronic hepatitis B and C. 809 55

Interferon-alpha induces remission in 30% to 40% of patients with chronic hepatitis B, but its effect on hepatic connective tissue turnover has not been well documented. We studied the changes in serum procollagen III propeptide and laminin-P1 peptide (Lam-P1) in 33 patients with chronic hepatitis B (11 nontreated controls and 22 treated patients) during a 4-mo randomized trial of interferon-alpha. Liver biopsy specimens were obtained at the start of treatment and 12 mo later. Liver biochemical tests, procollagen III propeptide, laminin-P1 peptide and hepatitis B virus DNA polymerase were determined before treatment with interferon was begun (mo -3), at the initiation (0 time) and completion of treatment (mo 4) and also at 8, 12 and 18 mo. Treated patients were classified as "responders" and "nonresponders" on the basis of clearance of HBV e antigen from serum. There were no significant changes in the control group, whereas the responders had persistent decreases in ALT, AST, hepatitis B virus dna polymerase, procollagen III propeptide and laminin-P1 peptide. The nonresponders had transient ALT, AST and hepatitis B virus dna polymerase reductions that returned toward baseline levels during follow-up, but procollagen III propeptide and laminin-P1 peptide persisted below the baseline at mo 18. Significant correlations between procollagen III propeptide and laminin-P1 peptide with ALT, AST and liver histologic specimens were noted at baseline but not after 12 mo. Changes in procollagen III propeptide levels also correlated with changes in AST, ALT and liver histologic specimens.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Decrease in serum levels of markers of hepatic connective tissue turnover during and after treatment of chronic hepatitis B with interferon-alpha. 813 56

The hepatitis B virus is a member of an unusual family of noncytopathogenic, hepatotropic DNA viruses--the hepadnaviruses. The complete virus comprises a lipoprotein coat, the hepatitis B surface antigen, enveloping a nucleocapsid core that contains a small, circular DNA molecule. Four open reading frames have been identified on the hepatitis B virus DNA genome. They encode seven proteins, including a hepatitis B virus DNA polymerase molecule with reverse transcriptase activity. The replication of the virus resembles that of retroviruses and occurs predominantly but not exclusively in hepatocytes. Virus variants involving genomic mutations have been identified. Testing for hepatitis B surface antigen permits detection of many but not all acutely infected patients. Diagnosis of acute infection rests on the identification of IgM antibodies to the hepatitis B core antigen. Antibody to hepatitis B surface antigen appears in serum during the convalescent phase of hepatitis B virus infection. It is the neutralizing, protective antibody largely responsible for immunity to reinfection. In persistent infection hepatitis B surface antigen is present, antibody to hepatitis B core antigen is predominantly an IgG antibody, antibody to hepatitis B surface antigen is not detectable or is present in very low titers and viral replication may be active. Persistent infection leads to an asymptomatic carrier state, chronic hepatitis, cirrhosis and hepatocellular carcinoma. No specific treatment exists for acute hepatitis B virus infection. Current data indicate that approximately 50% of adults who have chronic infection achieve virologic, biochemical and histologic remission from treatment with alpha-2b-interferon.
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PMID:Hepatitis B today: clinical and diagnostic overview. 832 12

Ribavirin is a nucleoside analog that inhibits the replication of many DNA and RNA viruses. To evaluate the efficacy of oral ribavirin, we randomly assigned 24 HBeAg-positive patients with chronic active hepatitis to a 12-wk course of treatment with 0.8 to 1.0 gm/ribavirin day, 3 mU interferon-beta three times a week intravenously or a combination of those drugs. Ribavirin, alone and in combination with interferon-beta, decreased hepatitis B virus levels in most patients, and mean serum hepatitis B virus DNA and DNA polymerase levels at the end of treatment were approximately half of baseline levels (p < 0.05). Interferon alone exerted the most inhibitory effect on hepatitis B virus activity (p < 0.01). During ribavirin treatment, changes in serum aminotransferase values varied considerably and the mean values did not change significantly, although interferon alone and the combination of interferon and ribavirin were associated with significant reductions in serum aminotransferase activities. Ribavirin was well tolerated, but we transiently reduced the dosage in two cases because of mild hemolytic anemia, although all patients completed the treatment schedule. The combination of interferon and ribavirin did not appear to result in greater toxicity. During the follow-up period (6 to 9 mo), HBeAg and hepatitis B virus DNA disappeared in one patient treated with ribavirin, in two treated with interferon and in two given the combination. These results indicate that ribavirin suppresses hepatitis B virus replication, although its effect is less than that of interferon, and that it may be useful as adjunctive therapy for chronic hepatitis B.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pilot study of ribavirin and interferon-beta for chronic hepatitis B. 834 55

Altered expression of asialoglycoprotein (ASGP) receptors on hepatocytes has been reported during hepatic neoplasia mostly in animal models. In this study, we examined immunohistochemically the distribution of the ASGP receptor in humans with various liver diseases, including ten cases of hepatocellular carcinoma (HCC). In livers of acute hepatitis, chronic hepatitis, cirrhosis and the non-cancerous tissues (mostly cirrhosis) adjacent to HCC, the receptor was present in its normal distribution, i.e. mostly along the sinusoidal margin and partly on the lateral surface of hepatocytes. In four of six well-differentiated HCCs, the receptor was also normally distributed on the plasma membrane; by immunoelectron microscopy, it was seen in the endoplasmic reticulum and in pits in the plasma membrane but not on bile canaliculus-like structures, suggesting that it was synthesized, transported, and integrated into the plasma membrane in a polar manner. In contrast, there was no surface expression of the ASGP receptor in the remaining six HCCs (two well-differentiated and four poorly differentiated). In two of the poorly differentiated HCCs, the receptor, although absent from the cell surface, was prominent in the endoplasmic reticulum, suggesting disturbed transport of the ASGP receptor to the cell surface. When we examined proliferative activity of HCCs by immunohistochemical labeling of DNA polymerase alpha, HCCs with high percentages (above 30%) of DNA polymerase alpha-positive cells had lost the cell-surface expression of the receptor. Thus, the expression of the ASGP receptor in human HCC appears to be closely related to differentiation and proliferative activity of the tumor cells.
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PMID:Distribution of asialoglycoprotein receptor in human hepatocellular carcinoma. 838 55


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