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)

Twelve male patients with chronic hepatitis B were treated by the combination of recombinant human alpha-interferon and cyanidanol. They received 3 million units of interferon twice a week and 2,250 mg of cyanidanol daily for 24 weeks. Four patients had sustained clinical improvement in which hepatitis B e antigen and DNA polymerase disappeared from sera and aminotransferase activities fell to normal levels. Elevated pretreatment aminotransferases were associated with the response to therapy. Also, decreased number of OKT4-positive cells prior to treatment were observed among responders. Side effects were minimal and all patients tolerated treatment on an outpatient basis. Twice weekly administration of recombinant leukocyte interferon with cyanidanol may be effective in treating chronic hepatitis when patients are appropriately selected.
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PMID:Treatment of chronic hepatitis B with recombinant leukocyte interferon and cyanidanol. 335 Feb 78

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

Eleven patients with hepatitis B (HB) virus related chronic hepatitis were treated with recombinant interleukin 2 (rIL 2). Two hundred and fifty to 1000 units were given intravenously once daily for seven to 28 days. In five patients serum glutamic pyruvic transaminase activity rose transiently. Six patients showed a decrease in HBV DNA polymerase. One patient lost HBs, e antigens (Ags) and gained anti-HBs, e antibodies, while one lost HBs Ag and another HBe Ag. 2'-5' oligoadenylate synthetase activity in mononuclear cells in the peripheral blood did not change during treatment. The number of CD4 positive (helper/inducer) cells and natural killer cell activity increased after therapy (p less than 0.05, p less than 0.01). These results suggest that rIL 2 acts as an immunomodulatory agent enhancing host immune activity and may be beneficial in patients with chronic HB virus infection.
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PMID:Effect of recombinant interleukin 2 on hepatitis B e antigen positive chronic hepatitis. 350 87

Five patients with chronic hepatitis B were treated with 8-day courses of leukocyte (alpha) interferon (5 X 10(6) U/day) and with 8-day courses of recombinant fibroblast (betaser) interferon at dosages of 5 X 10(6), 35 X 10(6), and 105 X 10(6) U/day. Inhibition of hepatitis B virus replication as evidenced by a decrease in DNA polymerase (DNAP) activity was seen during all treatment courses. Equivalent reduction in DNAP was seen from the low-dose alpha and beta ser regimens, but beta ser interferon at 35 X 10(6) U/day achieved a significantly greater decrease in DNAP activity than did the low-dose regimens. In no patient, however, was permanent loss of DNAP noted. Because of dose-limiting toxicity, only two patients were escalated to the 105 X 10(6)-U/day dosage level. Transient proteinuria was noted in two patients while they were receiving interferon. This has not been noted in other patients receiving this preparation and could not be explained by the development of anti-interferon antibodies. This study has defined an appropriate dosage for future longer-term trials of this agent alone and in combination with other antivirals for the treatment of chronic hepatitis B.
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PMID:Preliminary trial of recombinant fibroblast interferon in chronic hepatitis B virus infection. 352 20

Treatment of chronic hepatitis B (CHB) with human leukocyte interferon (IFN-alpha) was studied in terms of increase of 2',5'-oligoadenylate (2-5A) synthetase activity in peripheral blood lymphocytes (PBL) after IFN-alpha administration. The 2-5A synthetase activity in PBL increased to a maximum 16-24 h after IFN-alpha injection and then gradually decreased, while serum HB virus DNA polymerase (HBV-DNAP) activity, which corresponds to the amount of HBV virions in the serum, decreased to a minimum after about 48 h. Increase in 2-5A synthetase activity was followed about 1 day later by decrease in DNAP activity. Furthermore, of 9 patients treated with IFN for at least 22 weeks and observed for over 1 year after IFN treatment, the effective 5 cases in which HBeAg disappeared during IFN therapy and did not reappear showed rather high increases in 2-5A synthetase activity, whereas the ineffective 4 cases in which HBeAg remained positive at the end of IFN therapy showed little increases in enzyme activity. The present study suggests that prescreening by 2-5A synthetase assay before IFN therapy should be useful for obtaining better results in IFN treatment of CHB patients.
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PMID:2',5'-Oligoadenylate synthetase activity in peripheral blood lymphocytes as a clinical marker in interferon therapy for chronic hepatitis B. 358 79

During a prospective study of acute symptomatic viral hepatitis, started in 1978, 664 consecutive adult patients, including 223 drug abusers, fulfilled the diagnostic criteria (anti-HBc IgM positivity) for acute type B hepatitis. In order to evaluate the outcome of the disease, 443 patients were followed for up to 12 months after the onset. 2.4% of the infections became chronic; the rate did not significantly differ between drug addicts and non-drug abusers, suggesting that chronic hepatitis is a rare complication of acute symptomatic hepatitis type B. Ongoing liver damage after clearance of HBsAg from serum was observed in drug abusers only (14% of the cases). Clinical, biochemical and virological features of the acute phase in patients with ongoing infection were compared with those of uncomplicated cases. Anicteric hepatitis and lower transaminase values were significantly (p less than 0.05) associated to a chronic evolution of the disease, as well as a higher prevalence of HBV-DNA, DNA polymerase and HBcAg positivity in serum. Testing HBV-DNA and DNA polymerase early in the course of the infection appeared to be of high predictive value for the subsequent outcome of the illness.
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PMID:Chronic evolution of acute hepatitis type B: prevalence and predictive markers. 371 May 94

The lymphocyte subsets in the peripheral blood and in liver biopsies from 4 patients with chronic hepatitis B obtained about 2-7 weeks before and after treatment with adenine arabinoside (Ara-A) were studied by a peroxidase-labeled antibody method using monoclonal antibodies against Leu-1, Leu-2a, Leu-3a, Leu-7 and Leu-10 antigens. In the peripheral blood, the percentage of Leu-2a+ (cytotoxic/suppressor) cells was significantly reduced and the ratio of Leu-3a+ (helper/inducer) to Leu-2a+ cells was increased after the treatment with Ara-A. In the liver biopsies, the numbers of Leu-1+ (pan T) and Leu-2a+ cells were significantly decreased after the treatment with Ara-A. As a result, the Leu-3a+/Leu-2a+ ratio was significantly elevated in the liver after the therapy. The majority of lymphocytes distributed at sites of hepatocytic necrosis were positive for Leu-2a. The reduced numbers of Leu-1+ and Leu-2a+ cells after the treatment were mainly due to the decrease of these cells infiltrating to the sites of hepatocytic necrosis. The numbers of other subsets (Leu-3a+, Leu-7+ and Leu-10+) changed without any specific tendency both in the peripheral blood and in the liver biopsies after the treatment. With respect to viral replication, most of the patients showed a decrease of serum DNA polymerase activity or demonstrable intrahepatic HBsAg and HBcAg after the treatment. These data suggest that T cell-mediated cytotoxicity against HBV-infected hepatocytes is diminished after treatment with Ara-A.
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PMID:Effects of adenine arabinoside on cellular immune responses in patients with chronic hepatitis B. 373 54

Adenine arabinoside is an antiviral agent which has been used in a number of clinical studies for the treatment of chronic infections with hepatitis B virus. In order to better understand its effects and mode of action, we treated ducks chronically infected with duck hepatitis B virus with a 2-week course and monitored the effects of the drug on viral replication by studying duck hepatitis B virus DNA in liver and serum using molecular biological techniques. We found the drug to be effective in ducks only at much higher doses than those used in humans. At high doses, adenine arabinoside had a dose-related inhibitory effect on viral replication during treatment, but there was a rapid return toward baseline values soon after the cessation of treatment. The supercoiled form of viral DNA was found to be most resistant to adenine arabinoside therapy, and the drug had a disproportionate inhibitory effect on viral plus (noncoding) strand synthesis. We conclude that adenine arabinoside likely exerts its effect in hepadna virus infections predominantly through inhibition of viral DNA polymerase. On the basis of our current study and previous trials in hepatitis B virus-infected patients, we predict that adenine arabinoside will not efficiently eliminate viral replication in chronic hepadna virus infection, when used as the sole therapeutic modality. Adenine arabinoside may have a role to play as an adjunct to immunomodulation or interferon therapy in chronic hepatitis B virus infection in man.
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PMID:Effects of adenine arabinoside on serum and intrahepatic replicative forms of duck hepatitis B virus in chronic infection. 380 2

Large doses of recombinant leukocyte A interferon were administered to 20 patients with deoxyribonucleic acid polymerase- and hepatitis B e antigen-positive chronic hepatitis B to study the maximum tolerated dose, its pharmacokinetics, and its antiviral activity. The first group of 5 patients received a constant dose of 36 X 10(6) U/day for 28 consecutive days. When it was well tolerated, the second, third, and fourth groups (5 patients each) received 50, 72, and 100 X 10(6) U/day, respectively. All 20 patients completed the 28-day treatment. Hourly and daily profile of serum interferon level showed a dose-dependent effect with an increasing dosage, and cumulative effects during the treatment. The mean peak serum interferon concentration ranged from 93 U/ml on day 1 in the first group to 1271 U/ml on day 28 in the fourth group. Inhibition of serum deoxyribonucleic acid polymerase activity and hepatitis B virus-deoxyribonucleic acid during the treatment was compared between the groups with low doses (36 and 50 X 10(6) U) and high doses (72 and 100 X 10(6) U). Low doses of interferon suppressed deoxyribonucleic acid polymerase activity to the same extent as did the high doses. Prednisolone withdrawal was combined with interferon in 5 patients. Three patients treated with such combination became seronegative for hepatitis B e antigen during the treatment, whereas all 15 with interferon alone remained seropositive. These results suggest that a maximum antiviral effect of recombinant leukocyte A interferon is below the maximum tolerated doses.
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PMID:Recombinant leukocyte a interferon treatment in patients with chronic hepatitis B virus infection. Pharmacokinetics, tolerance, and biologic effects. 397 31

We measured serum markers of hepatitis B virus replication in two HBsAg-, HBeAg-positive hepatitis B carriers with chronic active hepatitis and cirrhosis. The first of these patients was HBsAg-, HBeAg-, HBV DNA- and HBV DNA polymerase-positive initially and spontaneously lost HBV DNA polymerase and HBV DNA. During the HBeAg-positive, DNA polymerase-negative "window phase", an increase in viral replication, characterized by the reappearance of HBV DNA and HBV DNA polymerase occurred, together with an aggravation of the underlying chronic hepatitis. In the second HBsAg-, HBeAg-positive carrier, spontaneous fluctuations in HBV replication were associated with clinical deterioration. Delta agent and hepatitis A virus superinfection were excluded. These observations suggest that spontaneous low-grade fluctuations of HBV replication accompanied by an increase in the biochemical activity of the underlying chronic hepatitis can be observed in certain HBV carriers.
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PMID:Clinical and serological events accompanying changes in hepatitis B viral replication: case reports. 399 35


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