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)

Circulating complete and defective hepatitis B virus forms, as represented by full, DNA polymerase-positive and empty, DNA polymerase-negative Dane particles, respectively, were investigated in sera from patients with chronic hepatitis B virus infection and related to the presence of e antigen and antibody and to the histological findings on liver biopsy. Complete hepatitis B virus particles were detected in the serum of all patients postive for e antigen, their percentage ranging from 15 to 61% of the total Dane particle population. Although most of these cases had chronic persistent or chronic active hepatitis, complete viral particles were also found in serum of 3 healthy carriers of hepatitis B surface antigen who had e antigen. These results indicate that e antigen is a marker of active virus replication and support its association with infectivity. It is also associated with liver damage because production of complete virus is a feature of chronic hepatitis. In the presence of anti-e, detection of Dane particles in serum appeared to be related to the histological findings. Most of the healthy carriers had no Dane particles in serum, whereas 80% of the cases with chronic liver disease had circulating Dane particles. However, in contrast to the cases with e antigen, 98 to 100% of Dane particles in these cases appeared to be defective in nucleic acid material on electron microscopy after positive staining. All of the patients with chronic active hepatitis in this group had progressed to cirrhosis and it is possible that production of complete virus particles is reduced in the later stages of the illness.
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PMID:Full and empty Dane particles in chronic hepatitis B virus infection: relation to hepatitis B e antigen and presence of liver damage. 70 Mar 29

Studies conducted in 1970 and 1971 with heat-inactivated MS-2 serum revealed that this active immunizing procedure was associated with a protective effect, a more attenuated hepatitis B infection and a decreased hepatitis B carrier rate. More recent studies have revealed striking differences in the response of unimmunized and immunized persons following a parenteral exposure to the MS-2 strain of hepatitis B virus. Serial tests for the detection of hepatitis B surface antigen (HBsAg), DNA polymerase activity, serum transaminase (SGOT), antibody to HBsAg (anti-HBs) and antibody to hepatitis B core antigen (anti-HBc) revealed the following findings. In serosusceptible unimmunized persons HBsAg was detectable about 4 weeks after exposure, DNA polymerase activity at about 6 weeks, abnormal SGOT levels at about 8 weeks, anti-HBc at about 8-10 weeks, and anti-HBs usually after 20 weeks. In successfully immunized persons HBsAg, DNA polymerase activity, abnormal SGOT levels, and anti-HBc were not detectable, evidence of a booster response of pre-existing or non-detectable anti-HBs was observed one to two weeks after exposure. Studies by various investigators have revealed that anti-HBs is associated with protection and resistance to reinfection. In contrast, anti-HBc is not protective and does not correlate positively with either resistance to infection or recovery from infection. The availability of sophisticated biophysical and biochemical techniques has enabled several investigators to prepare candidate inactivated hepatitis B vaccines from purified preparations of HBsAg. The successful propagation of hapatitis B virus infection to susceptible chimpanzees has provided an excellent animal model for the evaluation of hepatitis B vaccines. At the present time various investigators are studying the immunogenic and protective effect of the vaccine in these animals. Prospects for the development of a vaccine for the prevention of viral hepatitis type B are encouraging. It is extraordinary that this objective will be achieved in spite of the failure to isolate the etiologic agent in tissue culture.
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PMID:Viral hepatitis type B: propects for active immunization. 120 71

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

We have studied antibodies (anti-pol antibody) against the polymerase gene product of hepatitis B virus by solid-phase enzyme immunoassay using synthetic peptides coded for by this gene. Sera from six patients with acute hepatitis B, 112 chronic hepatitis B virus carriers and six healthy individuals with naturally acquired immunity to hepatitis B virus were tested for anti-pol antibody. In acute hepatitis B virus infection, anti-pol antibody was detected in three of six patients. In chronic hepatitis B virus infection, anti-pol antibody was detected in 17 of 29 (59%), in 23 of 33 (70%) of cirrhotic patients and in 18 of 24 (75%) patients with cirrhosis complicated by hepatocellular carcinoma, compared with 4 of 19 (21%) asymptomatic carriers and 2 of 7 (29%) patients with chronic persistent hepatitis. Titers of anti-pol antibody were higher in cirrhotic patients with and without hepatocellular carcinoma than in patients with chronic active hepatitis. The presence of anti-pol antibody, however, had no relationship with hepatitis B virus-associated DNA polymerase activities and other viral replicative markers. As for sera from six healthy individuals with naturally acquired immunity to hepatitis B virus, two (33%) were positive for anti-pol antibody. These results indicate that the immune response toward the polymerase gene product is induced during acute and chronic hepatitis B virus infection. In chronic hepatitis B virus infection, anti-pol antibody may serve as a new marker indicative of a long period of hepatitis B virus-induced hepatitis.
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PMID:Detection of antibodies against the polymerase gene product in hepatitis B virus infection. 239 Oct 62

The effects of suramin, an antiparasitic agent, upon in vitro hepatitis B surface antigen production by the human hepatoma cell line PLC/PRF/5 and hepatitis B virus associated DNA polymerase activity in the serum of a chronically infected patient were examined. Treatment with suramin resulted in decreases in hepatitis B surface antigen production and hepatitis B-virus associated DNA polymerase activity. The decrease in hepatitis B surface antigen production was paralleled by a general decrease in hepatoma cell viability and cellular protein synthesis. Although the inhibitory effects of suramin for hepatitis B virus appear to be nonspecific as demonstrated in these two in vitro systems, the recently announced trial of suramin for the treatment of the acquired immunodeficiency syndrome should afford an unusual opportunity to evaluate the effectiveness of suramin in the treatment of chronic hepatitis B virus infection.
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PMID:Effects of suramin on in vitro HBsAg production by PLC/PRF/5 cells and hepatitis B virus DNA polymerase activity. 242 68

The effect of 2',3'-dideoxycytidine, a potent antiviral agent, which, following anabolic phosphorylation, inhibits the reverse transcriptase of the human immunodeficiency virus in vitro, was assessed in 16 Pekin ducks chronically infected with the duck hepatitis B virus. Nine ducks were given 11 mg/m2 of dideoxycytidine intravenously every 6 h, and 7 ducks received no treatment. Serum duck hepatitis B virus deoxyribonucleic acid and deoxyribonucleic acid polymerase activity decreased in every duck treated with dideoxycytidine. The mean inhibition of deoxyribonucleic acid polymerase and duck hepatitis B virus deoxyribonucleic acid on the third day of treatment measured 64% (p less than 0.01) and 73% (p less than 0.01), respectively. The inhibition of deoxyribonucleic acid polymerase persisted after treatment was stopped, and 4 ducks continued to show greater than 50% inhibition 12 days after stopping treatment. Duck hepatitis B virus deoxyribonucleic acid, which was measured in total cellular deoxyribonucleic acid extracted from liver biopsy specimens obtained before and on the last day of treatment with dideoxycytidine, showed an average inhibition of 96% in 3 ducks treated with dideoxycytidine, but showed no decrease in the remaining 5 ducks. Thus, dideoxycytidine has potent antiviral activity against duck hepatitis B virus and warrants further evaluation as an antiviral agent in the treatment of chronic hepatitis B virus infection in humans.
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PMID:Inhibition of duck hepatitis B virus replication by 2',3'-dideoxycytidine. A potent inhibitor of reverse transcriptase. 247 99

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

Ten young adult patients with chronic hepatitis B virus infection and positive hepatitis B e antigen and DNA polymerase (DNAP) levels were treated with alternating courses of seven to 28 days of 5 to 7.5 mg/kg of vidarabine monophosphate (adenine arabinoside monophosphate) and 28 days of human leukocyte interferon (IFN-alpha); three different regimens were given on an outpatient basis. All patients with a fall in their DNAP level, and the DNAP remained undetectable six months after treatment was stopped in one patient. The major side effect, which most often occurred in those patients receiving 7.5 mg/kg of vidarabine monophosphate, was severe muscular pains. This study demonstrated the feasibility of administering vidarabine monophosphate and interferon to outpatients. Based on data from this and other studies, it is now possible to use a relatively nontoxic regimen that includes 28 days of 5 mg/kg of vidarabine monophosphate in a larger controlled study to answer the question of efficacy.
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PMID:Vidarabine monophosphate and human leukocyte interferon in chronic hepatitis B infection. 617 74

The effect of interferon (IFN) on hepatitis B virus infection in patients with chronic active hepatitis is discussed. We can expect disappearance of DNA polymerase and HBeAG from serum by IFN administration. There seems to be no difference between IFN-alpha and IFN-beta in the effect on chronic hepatitis B virus infection. Female and those who with low pretreatment DNA polymerase activity are more susceptible to IFN treatment. With IFN alone, it is hard to expect a persistent disappearance of HBsAg. IFN therapy combined with other agents, such as adenine arabinoside, prednisolone, etc. must be considered in the future.
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PMID:[Effect of interferon on hepatitis B virus infection in patients with chronic active hepatitis]. 669 58

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.
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PMID:Failure to detect naturally occurring serum inhibitors of hepatitis B virus deoxyribonucleic acid polymerase. 676 9


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