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

---

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

The entity of chronic hepatitis has long been an enigma, and its treatment confusing. Recent studies have indicated the importance of excluding causes such as drugs, Wilson's disease and alpha 1-antitrypsin deficiency. After excluding such causes, there are 3 major groups--'autoimmune', hepatitis B, and non-A, non-B (NANB) in all of which an immunological basis for pathogenesis exists. The autoimmune group has been subdivided into a milder type (chronic persistent hepatitis) and a more severe type (chronic active hepatitis) on histological grounds. Corticosteroids are indicated in chronic active hepatitis if cirrhosis or bridging necrosis is present. However, corticosteroids are contraindicated in disease due to the hepatitis B virus where chronic active hepatitis correlates with the presence of replicating virus (serum positive for e antigen, DNA polymerase and HBV-DNA), and in such cases antiviral agents and immunomodulation are being studied. Very little is known about NANB hepatitis in the absence of an assay and there may be more than a single agent. In hepatitis B, the development of serological markers, molecular probes (HBV-DNA), natural animal hepatitis with near-identical viruses, and delta antigen (a virus requiring co-infection with hepatitis B) have all extended our knowledge so dramatically that it is hoped that the enigma of chronic hepatitis will be solved when an assay for NANB hepatitis becomes available.
...
PMID:Chronic hepatitis. Aetiology and current management. 673 69

Sera of patients with past or ongoing hepatitis -B virus infection were tested for the presence of inhibitors of hepatitis -B virus-specific deoxyribonucleic acid (DNA) polymerase activity. None of the sera tested, which included those from anti-hepatitis B surface- and anti-hepatitis B core antigen-positive hemophiliacs, anti-hepatitis Bc antigen-positive hepatitis B surface antigen carriers, patients with hepatitis B surface antigen-positive chronic active hepatitis, hepatitis B surface antigen-positive hemodialysis patients, tumor patients with minimal hepatitis, patients with acute type B, type A, and type non-A, non-B hepatitis and individuals with autoimmune phenomena, contained inhibitors of DNA polymerase activity. This implies that the DNA polymerase test is not affected when utilized to quantitate DNA-containing Dane particles. In addition, there is no evidence that inhibitors of DNA polymerase activity play some pathogenic role in the course of hepatitis B virus infection.
...
PMID:Failure to detect naturally occurring serum inhibitors of hepatitis B virus deoxyribonucleic acid polymerase. 676 9

Using immunodiffusion, a major cross-reactivity had been previously demonstrated between hepatitis B(HBe/3 Ag) and the antigen reported in the serum on non A, non-B hepatitis patients, therefore redesignated NANBe Ag. By direct immunofluorescence a new antigen associated with, but distinct from, NANBe Ag has now been identified in the liver of 14/26 patients with NANB chronic active hepatitis. The homologous antibody was detected in the serum of these 14 patients. Behaving like HBc Ag and cross reacting with it by immunofluorescence, the new antigen was termed NANBc Ag. Anti NANBc also became detectable in serial acute phase and convalescence sera from 5/5 NANB Ag-positive posttransfusion hepatitis cases. Further characterization of NANBe and NANBc antigens achieved by fractionation of a NANB virus-infected liver showed NANBc Ag to be expressed on 22-25 nm HB core-like particles containing DNA polymerase activity. Cross-reactivity between NANBc and HBc antigens was confirmed by immunodiffusion. Liver-derived NANBe Ag identical to serum NANBe Ag exhibited the same physical properties as HBe/3 Ag and could be similarly released by disruption of the non-A, non-B, virus cores. These results indicate that hepatitis B and NANB virions not only share the same structure and DNA polymerase activity but are also antigenically related and belong to the same new class of DNA viruses.
...
PMID:Non-A, Non-B hepatitis virus: identification of a core antigen-antibody system that cross reacts with hepatitis B core antigen and antibody. 679 10

Complete and defective hepatitis B virus (HBV) particles in sera and hepatocytes were observed by electron microscopy for an understanding of the maturation process of hepatitis B virus. To distinguish Dane particles with or without DNA on the basis of staining density with uranyl acetate, Dane particles, purified from sera of asymptomatic carriers, and Dane particle cores, separated by ultracentrifugation in a metrizamide density gradient, were observed by electron microscopy. Complete cores at a low density (1.19 to 1.23 gm/cm3) were electron dense and incomplete cores at a high density (1.23 to 1.27 gm/cm3) were partially electron dense or empty. These findings demonstrated that the presence or absence of DNA is reflected by the electron density of the core. Our result, in which less than 10% serum Dane particles have full cores in ultrathin sections of the pellet, is in agreement with Gerin's finding that defective Dane particles are predominent in sera. Naked core particles and Dane particles in two biopsy specimens from patients with hepatitis B surface antigen, hepatitis B e antigen, and DNA polymerase-positive, chronic active hepatitis were classified into complete versus incomplete particles on the basis of electron density. Nine hundred and fourteen naked core particles were detected in nuclei and cytosol of 68 hepatocytes. One hundred and five core particles (11.5%) were electron dense and 809 core particles (88.5%) were partially electron dense or empty. Furthermore, 488 Dane particles were observed in the cisternae of the endoplasmic reticulum of these hepatocytes. Fifty Dane particles (10.2%) had full cores, and 438 Dane particles (89.8%) had partially full or empty cores. These findings suggest that DNA may be incorporated into about 1 to 10% of core particles when they are assembled in nuclei of hepatocytes. Morphologic differences in damage to hepatocytes containing various frequencies of full Dane particles were also studied, but no significant correlation was found between damage in hepatocytes and frequency of full Dane particles.
...
PMID:Full and empty particles of hepatitis B virus in hepatocytes from patients with HBsAg-positive chronic active hepatitis. 685 94

We examined the clinical significance of hepatitis Be antigenemia in 36 HBsAg positive pediatric dialysis and renal transplant patients. One hundred twenty-seven sera were tested for HBeAg and anti-HBe. Seventy-three sera (57%) from 29 patients (81%) contained HBeAg. The presence of HBeAg was associated with an increased titer of HBsAg (P < 0.005) and with the presence of the HBsAg carrier state (P < 0.001). HBeAg was found in 40% of specimens taken from dialysis patients, and in 70% of specimens from transplant patients (P < 0.001). No serum contained anti-HBe, although 28 of 29 sera (97%) tested had antibody to HBcAg. No association was found between the presence of HBeAg and serum aminoleucine transferase levels or the histologic evidence of chronic active hepatitis. Fifteen HBeAg negative sera from patients persistently positive for HBsAg were tested for HBV-specific DNA polymerase activity; 7 (47%) had significant activity. Since both HBeAg and DNA p are indicators of infectivity, many HBeAg negative sera from immunosuppressed HBsAg carriers may be infectious.
...
PMID:Hepatitis B infection in pediatric dialysis and transplant patients: significance of e antigen. 699 41

In 20 patients with HBsAg-and HBeAg-positive chronic active hepatitis, we determined the long-term effect of human leukocyte interferon as well as placebo treatment. During the 2-year follow-up period, HBsAg remained present in all patients, but the Dane particle markers HBeAg and DNA polymerase disappeared in two of 10 patients who had received interferon, and in 4 of 10 patients from the placebo group. Patients, with loss of HBeAg initially had HBs antigenemia for a longer period as well as a lower serum concentration of both HBsAg and DNA polymerase, fewer HbcAg-containing hepatocyte nuclei, and higher serum transaminase levels than did the patients in whom HBeAg persisted. Disappearance of Dane particle markers was associated with a decrease in HBsAg titer, appearance of anti-HBe, normalization of the serum transaminases, and morphological transition to inactive chronic hepatitis. We conclude that, in HBsAg- and HBeAg-positive chronic active hepatitis, disappearance of Dane particle markers occurs in approximately 30% of the patients within a 2-year period and that arrest of active viral replication is associated with loss of activity of chronic hepatitis. Treatment with human leukocyte interferon in the doses used in this study did not change the natural course of the disease.
...
PMID:Spontaneous disappearance of viral replication and liver cell inflammation in HBsAg-positive chronic active hepatitis: results of a placebo vs. interferon trial. 714 89

Hepatitis B virus (HBV) DNA was measured by a hybridization technique in the sera of three patients with HBsAg-positive chronic active hepatitis treated with fibroblast interferon (INF-beta). Although DNA polymerase activity was undetectable in all patients 2-4 weeks after the beginning of the treatment, HBV-DNA was always present in two patients and disappeared in the only patient who showed marked clinical and histopathological improvement of the liver disease after INF treatment. This suggests that serum HBV-DNA is a valuable marker to monitor during therapeutic trials of chronic HBV infection.
...
PMID:Effect of human fibroblast interferon (INF-beta) on hepatitis B virus DNA in serum. 715 Jul 11

8 children, known to have been hepatitis B surface antigen (HBsAg) and hepatitis B e antigen (HBeAg) positive for more than 6 months and with chronic active hepatitis on biopsy, received 2.5 mg levamisole/kg/day, 2 days a week for 6-18 months. In 6 of the 8 children transaminases normalized within 4-18 months of therapy, with seroconversion to antibody to HBeAg (anti-HBe) and disappearance of HBV-DNA polymerase from serum and of hepatitis B core antigen (HBcAg) from liver. In these cases liver biopsies taken after treatment showed histological regression to chronic persistent hepatitis. Two distinct patterns of response to levamisole were noted: patients having higher pretreatment transaminase levels and lower expression of HBcAg in the liver showed an early transaminase normalization and anti-HBe seroconversion with therapy, while in patients with less active disease and more diffuse HBcAg positivity in pretreatment liver biopsies, longer treatment periods were necessary to achieve these effects. Our results suggest that long-term levamisole therapy may be beneficial in HBeAg-positive chronic hepatitis type B.
...
PMID:Virological changes in chronic hepatitis type B treated with levamisole. 717

In eight patients with biopsy-confirmed chronic active hepatitis (CAH), hepatitis B e antigen (HBeAg) levels and DNA polymerase (DNA-P) activity were assayed three times a week for six weeks and once a week for another six weeks. HBeAg levels were rather constant, whereas DNA-P activity fluctuated. No correlation was observed between the quantities of HBeAg and DNA-P activity. An unexpected fluctuation in DNA-P activity was noted in all patients after an influenza vaccination.
...
PMID:Quantitative relationship between HBeAg and DNA polymerase activity in sera from patients with chronic active hepatitis during a three-month period. 722 20

Hepatitis B virus associated DNA polymerase activity, hepatitis b surface antigen (HBsAg), and serum aspartate aminotransferase were followed in 21 patients with chronic active hepatitis while immunosuppressive therapy (prednisone +/- azathioprine) was being withdrawn. In every case, DNA polymerase activity fell within 6-10 wk of decreasing treatment and became undetectable in 8 patients. This was usually accompanied by a fall in HbsAg titer and a transient rise in serum aspartate aminotransferase activity. Four additional patients with previously untreated HbsAg positive chronic active hepatitis were placed on prednisone for 12 wk. There was a rise in DNA polymerase activity and HBsAg titer with a fall in serum aspartate aminotransferase values during treatment. Upon discontinuing therapy, DNa polymerase activity fell dramatically in all 3 patients who completed their course of prednisone and became undetectable in 1. These findings suggest that immunosuppressive therapy has a potentiating effect on hepatitis B viral replication in patients with chronic active hepatitis.
...
PMID:Effects of immunosuppressive therapy on viral markers in chronic active hepatitis B. 728 93


<< Previous 1 2 3 4 5 6 Next >>

---