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)

Two patients referred for cancer chemotherapy were found to be chronic, asymptomatic hepatitis B surface antigen (HBsAg) carriers. They had normal serum aminotransferase levels, but their sera were positive for HGsAg and antibody to hepatitis B e antigen. Both patients developed acute, icteric hepatitis within 3 months of starting cycled chemotherapy. In both cases, the disease seemed to be caused by a recurrence of type B hepatitis; it was accompanied by a marked increase in HBsAg titer and the appearance of hepatitis B virus DNA and DNA polymerase in the serum. One patient had a second episode of acute hepatitis after a second course of chemotherapy, but both patients ultimately recovered and became seronegative for HBsAg. Thus, it seems that cancer chemotherapeutic agents can reactivate type B hepatitis in asymptomatic HBsAg carriers. This reactivation is most likely due to an increase in hepatitis B virus synthesis followed by a rebound in host immune responses to hepatitis B virus infection when therapy is stopped. Such a phenomenon could have important implications for the therapy of chronic hepatitis B virus infection.
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PMID:Reactivation of chronic hepatitis B virus infection by cancer chemotherapy. 706 60

The purpose of this study was to examine the association of circulating viral markers with ongoing liver disease in chronic hepatitis B virus infection. Hepatitis B e antigen (HBeAg) was significantly more likely to be associated with abnormal alanine aminotransferase (ALT) activity than was anti-HBe in a group of 102 HBsAg carriers (p less than 0.0001). Within this group, 57 carriers were analyzed for HBeAg, DNA polymerase, and hepatitis B surface antigen (HBsAg) titer, and the relation of each with abnormal ALT was determined. Both HBeAg and elevated DNA polymerase were much more likely to reflect abnormal ALT (p less than 0.00001 and 0.0006, respectively) than did HBsAg titer. Unlike previous studies, higher titers of HBsAg would not be demonstrated in healthy carriers when compared to HBsAg carriers with chronic elevation of ALT; nor were differences in titer appreciated between chronic active and chronic persistent hepatitis. The potential significance of these findings is discussed.
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PMID:The relationship of hepatitis B e antigen, DNA polymerase activity, and titer of hepatitis B surface antigen with ongoing liver injury in chronic hepatitis B virus infection. 709 Nov 31

Three patients with HBsAg-positive and DNA-polymerase-positive chronic hepatitis were treated with increasing dosages of intravenous acyclovir. A fall in DNA polymerase activity was seen with all courses of acyclovir but no dose-response relationship was evident. In only one patient did DNA polymerase fall to zero where it has remained for five months. Two out of 10 courses were associated with significant side effects with the highest dosages of acyclovir but these promptly resolved when the agent was stopped. Acyclovir's apparently partial and transient action suggests that it will not have a role in the treatment of chronic hepatitis B virus infection.
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PMID:Preliminary studies of acyclovir in chronic hepatitis B. 710 5

The hepatitis B virus is a member of an unusual family of noncytopathogenic, hepatotropic DNA viruses--the hepadnaviruses. The complete virus comprises a lipoprotein coat, the hepatitis B surface antigen, enveloping a nucleocapsid core that contains a small, circular DNA molecule. Four open reading frames have been identified on the hepatitis B virus DNA genome. They encode seven proteins, including a hepatitis B virus DNA polymerase molecule with reverse transcriptase activity. The replication of the virus resembles that of retroviruses and occurs predominantly but not exclusively in hepatocytes. Virus variants involving genomic mutations have been identified. Testing for hepatitis B surface antigen permits detection of many but not all acutely infected patients. Diagnosis of acute infection rests on the identification of IgM antibodies to the hepatitis B core antigen. Antibody to hepatitis B surface antigen appears in serum during the convalescent phase of hepatitis B virus infection. It is the neutralizing, protective antibody largely responsible for immunity to reinfection. In persistent infection hepatitis B surface antigen is present, antibody to hepatitis B core antigen is predominantly an IgG antibody, antibody to hepatitis B surface antigen is not detectable or is present in very low titers and viral replication may be active. Persistent infection leads to an asymptomatic carrier state, chronic hepatitis, cirrhosis and hepatocellular carcinoma. No specific treatment exists for acute hepatitis B virus infection. Current data indicate that approximately 50% of adults who have chronic infection achieve virologic, biochemical and histologic remission from treatment with alpha-2b-interferon.
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PMID:Hepatitis B today: clinical and diagnostic overview. 832 12


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