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)

The e determinant of hepatitis B surface antigen (HBS Ag) was found in 23 of 42 patients with chronic hepatitis B virus (HBV) infection. Presence of e antigen was associated with increases in DNA polymerase activity and in the number of circulating Dane particles. In the group with detectable e antigen, the average DNA polymerase activity was 367+/-78 counts per minute (cpm; mean+/-standard error [SE]), and the average number of Dane particles counted in electron micrographs was 4.4% of the total HBS Ag. In contrast, e antigen-negative patients had an average DNA polymerase activity of 40+/-6.9 cpm (P less than 0.1) and an average Dane particle count equal to 0.6% of the HBS Ag. The e antigen was detected in 68% of patients who were HBS Ag carriers or had persistent viral hepatitis and 40% of those with chronic active type B hepatitis. Thus, the presence of e antigen correlated with both the chronicity and presence of infectious HBV. However, it did not correlate with the type or severity of liver disease after HBV infection, since e antigen was present in both chronic benign and chronic aggressive hepatitis B infections.
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PMID:Correlation of e antigen, DNA polymerase activity, and Dane particles in chronic benign and chronic active type B hepatitis infections. 6 88

We assessed the prevalence and clinical significance of antibodies to hepatitis C virus among a cohort of 148 patients with chronic hepatitis B virus infection. Sixteen patients (11%) had anti-hepatitis C virus detectable by enzyme-linked immunoassay. The results from eight of these patients were positive by recombinant immunoblot assay. The results of recombinant immunoblot assay testing were not consistent; therefore the analysis of the patients' data was based on anti-hepatitis C virus enzyme-linked immunoassay results. Patients with chronic hepatitis B with anti-hepatitis C virus were more likely to be cirrhotic (44% vs. 21%) and to have decompensated liver disease (24% vs. 6%). Hepatitis B virus replication appeared to be suppressed in patients with both infections as measured by hepatitis B virus-associated DNA polymerase activity (mean = 2,055 vs. 2,555 cpm). Human immunodeficiency virus infection was more common in the anti-hepatitis C virus positive group (36% vs. 11%). Thus hepatitis C virus appears to suppress hepatitis B virus replication and to cause more severe liver disease in patients with chronic hepatitis B infection.
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PMID:The significance of antibody to hepatitis C virus in patients with chronic hepatitis B. 164 40

Serum DNA polymerase activity (DNA-P) was detected in 27.6 per cent of non-A, non-B (NANB) hepatitis patients, 8.7 per cent of patients with alcoholic liver disease (ALD), 8.6 per cent of hepatitis B surface antigen (HBsAg)-positive patients and 19.0 per cent of HBsAg-negative blood donors with elevated serum glutamic-pyruvic transaminase (SGPT) concentrations. In contrast, none of the patients with hepatitis A, drug-induced liver injury or non-alcoholic fatty liver had DNA-P in their sera in the acute phase of the illness. All HBsAg-positive samples with detectable DNA-P were strongly positive for hepatitis B virus (HBV) DNA, but the samples from patients with NANB hepatitis and ALD and HBsAg-negative blood donors had no HBV DNA. Sensitivity to actinomycin D showed the heterogeneity of DNA-Ps in HBsAg-negative blood donors; the enzyme activity of one type was inhibited by 100 micrograms/ml of actinomycin D, whereas the other was not. The preference for exogenous template primers of these DNA-Ps was different to those of HBV and human retroviruses. The results reveal the prevalence of serum DNA-P in NANB hepatitis patients and suggest that two distinct agents are relevant to the aetiology of NANB hepatitis.
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PMID:Prevalence and heterogeneity of serum DNA polymerase activity in patients with non-A, non-B hepatitis and HBsAg-negative blood donors with elevated SGPT. 212 73

Seventeen patients with chronic active type B hepatitis were treated with prednisone for 4 weeks. All were initially hepatitis B e antigen (HBeAg)-positive and 14 were DNA-polymerase-positive as well. In the follow-up period of 1 year, 10 patients became persistently negative for DNA polymerase and 11 cleared HBeAg from serum, while among 17 matched untreated controls only one lost DNA polymerase and HBeAg. However, 1 patient who was initially DNA-polymerase-negative and who lost HBeAg after treatment reactivated to HBeAg after 4 months and DNA polymerase appeared in his serum. He suffered prolonged exacerbation of liver disease after treatment and died of liver failure. Short-term corticosteroid therapy may be of value in patients with chronic active type B hepatitis, however, in some cases such treatment may be disastrous.
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PMID:Short-term corticosteroid therapy for chronic active hepatitis B. 229 53

Because the risk factors for human immunodeficiency virus (HIV) infection and hepatitis B (HBV) are similar and therefore coinfection is not uncommon, a detailed histological and immunohistochemical study of chronic hepatitis B infection in a group of 20 HIV positive Caucasian males (who did not have AIDS) and 30 HIV negative controls were undertaken. Using both the conventional histological classification and the Knodell histological activity index it was shown that HIV negative patients were more likely to have active disease and also more scarring than HIV positive patients. Hepatitis B surface antigen (HBsAg) expression was not significantly different between the two groups but expression of hepatitis Be antigen (HBeAg) and HBV-DNA polymerase was greater in those who were HIV positive. HIV positive patients are therefore more likely to have immunohistochemical markers of active viral replication, although histologically, liver disease is less severe. These findings have important implications for assessing the biopsy specimens in this group of patients and for treatment strategies aimed at improving their immune function.
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PMID:Histological and immunohistochemical study of hepatitis B virus in human immunodeficiency virus infection. 233 17

We have analyzed the immunomodulatory effect of 5 and 2 MU of recombinant interferon-gamma (rIFN-gamma) administered to 8 carriers of HBsAg with histologically proven chronic active liver disease. After the rIFN-gamma administration, T8 lymphocyte subsets showed a significant decrease (basal vs. 4 weeks, p less than 0.05) and T4/T8 ratios were higher than the basal values in 6/8 patients. Serum levels of the HLA class I-associated beta 2-microglobulin increased significantly in all patients within the first week of treatment, both with the high (p less than 0.01) and the low (p less than 0.05) rIFN-gamma dose. Then, differences between the two doses reached statistical significance (p less than 0.03). Similar results (p less than 0.05) were obtained by measuring the 2',5'-oligoadenylate (2-5A) synthetase activity, co-occurring with the decreases in HBV-DNA polymerase and HBV-DNA, although no differences were found between the two doses. In addition, levels of 2-5A synthetase correlated significantly with those of beta 2-microglobulin (r = 0.743, p less than 0.01). On the other hand, after the rIFN-gamma administration, all the patients had liver membrane antibodies (LMA) in their serum (p less than 0.05); only two patients (who were anti-HD positive) showed LMA at the end of the follow-up. rIFN-gamma has both antiviral and immunomodulatory effects in HBeAg carriers with chronic liver disease.
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PMID:Elevation of 2',5'-oligoadenylate synthetase activity and HLA-I associated beta 2-microglobulin in response to recombinant interferon-gamma administration in chronic HBeAg-positive hepatitis. 314 6

Liver biopsy specimens from 58 American patients with chronic type B hepatitis were investigated for the presence and distribution of the hepatitis B core (HBcAg) and surface (HBsAg) antigens by peroxidase-anti-peroxidase techniques. HBsAg was detected in 43 (77%) and HBcAg in 52 (90%) patients. HBcAg was present in 50 of 51 (98%) patients with hepatitis B e antigen (HBeAg) but in only two of seven (29%) of patients with antibody to HBeAg (anti-HBe). There was no correlation between severity of hepatitis or height of aminotransferase activities and the amount of HBsAg or HBcAg in hepatocytes but there was a positive correlation between amount of HBcAg and height of HBV-DNA and DNA polymerase activity in serum. Follow-up liver biopsies, taken 1 to 3 yr later, were available from 39 patients. HBcAg remained detectable in 25 of 26 patients with persistence of HBeAg but disappeared in 12 patients who had lost HBeAg. In nine patients, HBcAg was cytoplasmic as well as nuclear in distribution. Seven of these patients had an intense lobular hepatitis with marked elevations in aminotransferase activities. These findings indicate that the amount of HBcAg in liver correlates with the amount of serum hepatitis B virus as quantified by serum levels of DNA polymerase and HBV-DNA. The amount of nuclear HBcAg does not correlate with the severity of the liver disease, but the presence of cytoplasmic HBcAg usually reflects an active and severe ongoing hepatitis.
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PMID:Peroxidase-anti-peroxidase detection of hepatitis B surface and core antigen in liver biopsy specimens from patients with chronic type B hepatitis. 332 17

An assay for DNA polymerase reaction products using slab gel electrophoresis and autoradiography was compared with the spot hybridization technique for the detection of hepatitis B virus DNA in 317 blood samples. The former could identify the nature and size of DNA on electrophoresis, and reduce potentially false-positive results due to artifacts. Discordant results between the two methods occurred in 36 of 317 samples; 22 were positive by the spot technique alone, and 14 were positive by the analysis of DNA polymerase reaction products alone. However, the samples positive with the spot test alone showed weak radioactive signals on electrophoresis/autoradiography that were often interpreted as "inconclusive" by blind observations. Correlation of hepatitis B e antigen/antibody with hepatitis B virus DNA was studied in 91 patients with various chronic liver diseases. Discordant results, i.e., presence of the DNA in antibody positive sera, or its absence in the antigen positive sera, were obtained in 15 (19%) cases. Such patients tended to have advanced liver disease with fluctuating serum aminotransferase levels. Analysis of DNA polymerase reaction products by slab gel electrophoresis and autoradiography is not only sensitive, but is also as specific as the Southern blot technique in the detection of hepatitis B virus DNA in serum, and may prove useful in selected samples, especially where no cloned hepatitis B virus DNA is available, or in search of new hepatitis B virus-like viruses.
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PMID:Analysis of DNA polymerase reaction products for detecting hepatitis B virus in serum--comparison with spot hybridization technique. 392 78

Serum samples from 130 persons who were seropositive for hepatitis B surface antigen and who had various forms of accompanying liver disease were tested for immunoglobulin M (IgM) antibody to hepatitis B core antigen. In 99% of patients with hepatitis B antigen-positive chronic type B hepatitis, IgM antibody to hepatitis B core antigen was present. This antibody was not present in "healthy" hepatitis B surface antigen carriers and was detectable in only 30% of patients with delta hepatitis. Testing of serial sera from 38 patients with chronic type B hepatitis revealed that IgM antibody to hepatitis B core antigen persisted in patients who had evidence of persistent hepatitis B virus replication but ultimately disappeared in those patients who exhibited a sustained loss of serum markers of viral replication (hepatitis B virus deoxyribonucleic acid and deoxyribonucleic acid polymerase activity). These findings suggest that the presence of IgM antibody to hepatitis B core antigen in chronic hepatitis B surface antigen carriers indicates an active immune response to persistent viral replication.
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PMID:Immunoglobulin M antibody to hepatitis B core antigen in patients with chronic type B hepatitis. 400 16

In eight HBs and HBe antigen positive patients with chronic active liver disease, adenine arabinoside 5'-monophosphate (ARA-AMP) given, intravenously or intramuscularly, six or 12 hours, produced inhibition of viral replication. In five patients given a short course of therapy with 10 or 15 mg/kg/day this effect was transient and in two thrombocytopenia occurred. In three further consecutive cases given a longer course with 5 mg/kg/day after five days of the high dose, thrombocytopenia was not seen and inhibition of viral replication for up to 13 months occurred. These patients lost HBV-DNA polymerase activity, serum viral DNA and HBeAg, developed anti-HBe, and HBsAg concentrations decreased. A course of twice daily intramuscular ARA-AMP given for three to five weeks as an outpatient may be expected to produce a long-term reduction in infectivity.
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PMID:Successful treatment of HBs and HBeAg positive chronic liver disease: prolonged inhibition of viral replication by highly soluble adenine arabinoside 5'-monophosphate (ARA-AMP). 617 19


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