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)

In chronic viral type B hepatitis, the presence in the serum of pre-S proteins of hepatitis B virus (HBV) envelope reflects viral replication. As peripheral blood mononuclear cells (PBMC) are known to be target cells for HBV replication, the aim of our study was to investigate the clinical relevance of pre-S protein expression in PBMC. Fifty-seven patients with chronic type B hepatitis and HBs antigenemia were studied. Following separation using the Ficoll gradient, the PBMC were lysed and studied for pre-S proteins by Western blot. HBs Ag and HBc/e Ag were assayed in parallel by radioimmunoassay. HBs Ag was detected in PBMC in 86 percent of cases, HBc/e Ag in 28 percent of cases and pre-S proteins in 34 percent of cases. A statistically significant association was found between the presence of HBc/e Ag in PBMC and both the serum HBe Ag (chi 2 test, p less than 0.01) and the serum viral DNA/DNA polymerase (t test, p = 2.10(-4)). The pre-S protein expression in PBMC was significantly associated with higher levels of DNA/DNA polymerase activity (chi 2 test, p less than 0.05). The expression of pre-S proteins in PBMC appears therefore to correlate with the HBV viral replication phase. The HBc/e Ag and pre-S protein detection in PBMC therefore offers a reliable non invasive approach to tissular viral replication. The clinical relevance of pre-S testing in PBMC was illustrated by the study of 12 cases of chronic active hepatitis positive for anti-HBe but with no or low level of serum DNA polymerase activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Significance of the expression of pre-S proteins in mononuclear blood cells in chronic hepatitis caused by the hepatitis B virus]. 280 6

A 26-year-old patient developed HBsAg-, HBeAg-positive chronic active hepatitis arising from an acute infection 6 months earlier. Treatment with adenine arabinoside (Ara-A), 15 mg/kg/day administered as overnight infusions for three weeks, resulted in clinical and complete biochemical remission with normalisation of aminotransferases, loss of HBsAg, HBeAg and DNA polymerase, and appearance of Anti-HBs during follow-up for 9 months. Treatment of chronic hepatitis B infection using Ara-A for several weeks may be especially effective when initiated early in the course of the disease.
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PMID:Treatment of HBsAg-,HBeAg-positive chronic active hepatitis with adenine arabinoside. A case report with clinical remission and seroconversion to anti-HBs. 286

We have investigated the efficacy of recombinant alpha-interferon treatment of chronic hepatitis B virus (HBV) infection in two therapeutic trials. Forty-four patients positive for HBsAg, HBeAg, DNA polymerase and HBV-DNA were studied. Fourteen carriers were treated in the first trial with doses ranging from 18 to 50 million units (mu)/m2 3 times per week. Six of 14 treated carriers (43%) have a sustained loss of HBeAg, HBV-DNA and DNA polymerase. Four lost HBsAg (29%). Two of 11 (18%) untreated carriers lost HBeAg, but none lost HBsAg (P = 0.05). Nineteen patients were entered in a second trial to assess dose response. Fourteen were treated with doses ranging from 2.5 to 10 mu/m2. Five patients were untreated. Two treated patients seroconverted to anti-HBe, and a third cleared HBsAg and seroconverted to anti-HBs. None of the controls was anti-HBe-positive. Thus 9/28 (32%) carriers have lost replicating HBV versus 2/16 (13%) of untreated patients. Elevated pretreatment serum ALT concentrations and severe chronic active hepatitis were associated with inhibition of viral replication in treated patients suggesting that seroconversion may require an appropriate host response. The efficacy of recombinant interferon is restricted, but it may be of benefit in a proportion of carriers.
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PMID:Recombinant leucocyte interferon treatment of chronic hepatitis B. An analysis of two therapeutic trials. 329 8

A randomized controlled study of one course of vidarabin was carried out in 30 patients with HBs Ag, HBe Ag, DNAp, positive chronic active hepatitis: 15 patients were treated with vidarabin given intravenously (15 mg/kg/day for 7 days then 7.5 mg/kg/day for 14 days); the other 15 patients received a placebo for 21 days. During treatment, DNA polymerase activity fell dramatically in 13 treated patients and in no controls (p less than 0.001). Six months after inclusion, ALT normalization was observed in 40 p. 100 of the treated patients and 6 p. 100 of the controls (p less than 0.05), a decrease in inflammatory activity on liver biopsies was observed in 70 p. 100 of the treated patients and 20 p. 100 of the controls (p less than 0.05), a permanent lost of DNA polymerase and of HBe Ag occurred in 33 p. 100 and 13 p. 100 of the treated patients and 20 p. 100 and 7 p. 100 of the controls, respectively. In addition, a second course of vidarabin was administered to the 12 patients who were still HBe Ag positive 6 months after the first course. During the next 6 months, 8 patients lost DNA polymerase and 4 lost HBe Ag. Altogether, the final score of durable inhibition of HBV replication was 11/15 (73 p. 100) within one year. The above results demonstrate that one course of vidarabin can significantly improve ALT and liver inflammatory activity but the effect upon HBV replication is only transient. A second course does however increase efficacy on HBV replication without additional side effects.
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PMID:[Vidarabine treatment of chronic active hepatitis associated with hepatitis B virus multiplication. A randomized multicenter study]. 330 17

Twelve hepatitis B surface antigen (HBsAg), hepatitis B e antigen (HBeAg), hepatitis B virus DNA polymerase (HBV-DNAp) and hepatitis B virus DNA (HBV-DNA) positive patients with chronic active hepatitis (CAH) were treated with doses of either 20 X 10(6) IU/m2 or 10 X 10(6) IU/m2 body surface of recombinant interferon (rIFN)-alpha-2A, I.M., twice a week, during a period of 6 months. No appreciable differences with respect to clinical history, liver function tests and markers of HBV replication between the two groups were apparent at the time of entry into the trial. At the third month of treatment HBV-DNAp became negative in 10 out of 12 patients (83%). After a 15-month follow-up, HBV-DNAp, HBV-DNA and HBeAg were negative in 7 out of 12 patients (38%) (responders). Furthermore, at 24 months, 2 non-responder patients became HBV-DNA and HBV-DNAp negative and one responder lost serum HBsAg. In addition, HBsAg concentration, GPT level and histological Knodell's index decreased significantly in the responder patients, while no changes were observed in non-responders. Five out of six patients who received a low rIFN dose responded to the treatment, and only 2 out of 6 with a higher dose. No unacceptable toxicity was noted in any of the 12 patients. All of them completed the course of treatment. The results suggest that long-term rIFN-alpha-2A therapy has an antiviral effect in CAH due to HBV infection and is well tolerated.
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PMID:Prolonged (6 months) treatment of chronic hepatitis B virus infection with recombinant leukocyte A interferon. 343 94

Suramin has recently been shown to inhibit the activity of the duck hepatitis B virus DNA polymerase (DHBV DNAp) in vitro. However, we found no demonstrable in vivo suppression of human hepatitis B virus DNA polymerase (HBV DNAp) activity in three male patients with severe chronic active hepatitis. Suramin treatment resulted in prolongation of the prothrombin time in all cases and a rise in bilirubin in two and it may have led to haemorrhage from oesophageal varices in one patient and to hepatic encephalopathy in another. Its use in chronic hepatitis is not recommended.
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PMID:Suramin treatment for chronic active hepatitis B--toxic and ineffective. 349 74

Five patients with HBe antigen-positive chronic active hepatitis were treated with recombinant interleukin 2 (r-IL2) for 3 to 4 wk. r-IL2 inhibited HBV replication during therapy as judged by decrease of serum DNA polymerase activity. Two of five patients lost HBeAg from serum. Furthermore, characteristic increases of serum aminotransferase were observed during r-IL2 therapy. This rise might have been mediated by enhanced immune responses to hepatitis B virus and increased rate of lysis of the infected hepatocytes. No consistent changes in immune markers such as OKT4 positive cells or OKT8 positive cells were demonstrated during or after the therapy. The activities of natural killer cells gradually increased during therapy, although they tended to decrease within 1 wk after the start of r-IL2 injections. In two responders who lost HBeAg from serum, the natural killer activity was high before the therapy, compared with nonresponders. Furthermore, the percentage of OKT4-positive cells in the responders was increased within 1 to 2 wk after starting r-IL2 injections. These findings suggest that the responders might be immunologically different from the nonresponders. Recombinant-IL2 therapy over short periods did not result in complete clearance of hepatitis B virus. Further studies with high doses of r-IL2 given over longer periods are warranted.
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PMID:Effects of human recombinant interleukin 2 in patients with chronic hepatitis B: a preliminary report. 349 71

To determine the antiviral effect of recombinant-interferon (rIFN)-alpha in hepatitis B virus (HBV) chronic infection, a controlled study was carried out. A total of 20 HBsAg chronic carriers (18 chronic active hepatitis and 2 chronic persistent hepatitis) were included. All of them had remained HBeAg, HBV-DNA and HBV-DNA polymerase (HBV-DNAp) positive at least six months before treatment. The patients were randomly assigned to two groups: control (n = 10), and treatment (n = 10). A dose of 5.5 megaunits of rIFN-alpha/m2 body surface was administered every day for 21 days (induction) and twice a week for six months thereafter (maintenance). No basal differences were observed between the two groups. No case of intolerable toxicity was observed. One treated patient died in a car crash in the second month. At the end of the first week of therapy, 7/10 (70%) of the treated patients became HBV-DNAp negative. However, in the fifth month only 2 patients remained HBV-DNAp negative and also became HBV-DNA and HBeAg negative. In contrast, no changes in viral markers among control cases were observed. In conclusion, rIFN-alpha has an antiviral effect on chronic HBV infection; however, the induction plus maintenance schedule is not useful to obtain a permanent effect.
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PMID:A controlled study of treatment with recombinant interferon alpha in chronic hepatitis B virus infection: induction and maintenance schedules. 350 Dec 74

Short-term prednisolone therapy was instituted on 27 patients with chronic active hepatitis (CAH) type B, in an attempt to induce seroconversion from hepatitis B e antigen (HBeAg) to the corresponding antibody (anti-HBe). Patients with CAH received a four-week regimen of prednisolone with daily dosage tapering from 40 to 10 mg (total 700 mg). Within one year after the withdrawal of prednisolone, 19 (70%) lost HBeAg and 11 of them (41% of the total) developed anti-HBe, at rates significantly higher than 3 (12%) and 1 (4%) who spontaneously showed respective serological changes among 26 matched controls during one year (p less than 0.001). Within two years after the withdrawal, 21 (78%) lost HBeAg and 19 (70%) developed anti-HBe, in contrast to 6 (23%) and 2 (8%) of controls who showed respective changes during that period (p less than 0.001). Seroconversion to anti-HBe was invariably accompanied by clinical and biochemical improvements along with loss of DNA polymerase from circulation. Elevation in transaminase levels, reflecting the rebound of steroid withdrawal, always heralded and appeared to be required for the seroconversion, but serious aggravation of hepatitis was not encountered in any of the patients.
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PMID:Short-term prednisolone for inducing seroconversion from hepatitis B e antigen to antibody along with clinical improvement in patients with chronic active hepatitis type B. 362 61

The detection of HBe antigen (HBeAg) in the sera of chronic HBV carriers is classically used as a marker of viral replication and therefore of development and infectivity of the disease. On this basis, it was used for the selection of patients for antiviral treatment. However, discrepancies between the presence of HBeAg and signs attesting to viral replication, namely HBV DNA and DNA polymerase, have been reported. We attempted to determine the prevalence of markers of viral replication in a group of patients with chronic active hepatitis associated or not with cirrhosis. All 41 patients were HBs Ag carriers; HBe Ag was present in 36 (88 p. 100), and HBV DNA in 28 (68 p. 100). A statistically positive correlation was found between the presence of cirrhosis and the absence of viral replication. In spite of the detection of HBe Ag, no direct signs of viral replication were observed in 30 p. 100 of patients, mainly those with cirrhosis. Therefore it is clear that the detection of HBe Ag alone cannot be considered as a sign of viral replication. Direct signs of viral replication should help to select patients for antiviral therapy, which should be started before the occurrence of cirrhosis.
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PMID:[HBe antigen and B virus DNA in patients with chronic active hepatitis]. 380 9


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