Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eight patients with chronic hepatitis B infection (seven with chronic active hepatitis and one with chronic persistent hepatitis) were treated with daily intramuscular injections of human leucocyte interferon for periods of 5 to 8 weeks and in one case for 5 months. In one patient there was a marked fall in virus-associated DNA polymerase activity and in the number of DNA containing viral particles during each of two courses of interferon. Hepatitis Be antigen (HBeAg) also disappeared, the aspartate transaminase levels fell and liver histology improved. In the four other patients with detectable DNA polymerase activity there was an early fall but this was transient and in one of these patients there was a continuing rise in activity despite treatment. One other patient became HBeAg negative but hepatitis B surface antigen (HBsAg) titres were mostly unaffected by treatment. A marked decrease in T-lymphocyte mediated cytotoxicity towards HBsAg coated target cells was demonstrated and raises the possibility that an immunosuppressant action of interferon may offsets its direct anti-viral action but may also account for the improvement in liver function which occurred in some patients.
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PMID:Effects of human leucocyte interferon on hepatitis B virus replication and immune responses in patients with chronic hepatitis B infection. 50 26

A radioimmunoassay for hepatitis e antigen (HBeAg) and antibody to e (anti-HBe) was developed and sera of 71 asymptomatic chronic carriers of hepatitis B surface antigen (HBsAg), in 44 of whom liver biopsy was obtained, were tested. In addition, testing for Dane particle associated DNA polymerase activity was performed in all sera. HBeAg was detected in 14 subjects (19.7%) and anti-HBe in 46 (64.8%). The highest proportion of HBeAg positivity (40%) was found among carriers with histological evidence of chronic hepatitis, whereas anti-HBe was present in 80% of carriers with normal liver histology, in 58% of carriers with non-specific reactive hepatitis and in 60% of carriers with chronic liver lesions. DNA polymerase activity was present in 92.8% of sera positive for HBeAg, in 13% of sera positive for anti-HBe, and in 9% of sera negative for both markers. Our results demonstrate that not all HBsAg carriers reactive to HBeAg show evidence of chronic hepatitis nor, conversely, that anti-HBe is invariably associated with the healthy carrier state of HBsAg. Finally, circulating Dane particles, as revealed by the presence of serum specific DNA polymerase activity, may also be present in anti-HBe positive sera other than those of some HBsAg carriers lacking both HBeAg and anti-HBe.
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PMID:Radioimmunoassay in the detection of the hepatitis B e antigen/antibody system in asymptomatic carriers of hepatitis B surface antigen. Correlation with serum Dane particle associated DNA polymerase activity. 54 99

HBV has been shown to be responsible for a broad spectrum of disease in infants although most are asymptomatic carriers with mild transaminase elevation and unresolved hepatitis on liver biopsy. Maternal-infant transmission is responsible for most infections. Blood product infusion should become less significant. Acute maternal hepatitis in the perinatal period results in asymptomatic infant infections at rates far exceeding transmission from asymptomatic carrier mothers. Carrier mothers with the e-antigen or HBV-associated DNA polymerase transmit infection more readily than do carrier mothers without these HBV markers. The presence of maternal anti-e may be protective. Intrapartum and postpartum transmission occurs more often than transplacental infection. For this reason attempts at prophylaxis with immune serum globulin administered in the newborn period should be further evaluated.
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PMID:The infant and hepatitis B virus infection. 60 64

Hepatitis B surface antigen (HBs Ag) and associated particles, e antigen (e Ag) and DNA polymerase are unevenly distributed during Cohn's cold ethanol fractionation of plasmas positive for these markers of the hepatitis B virus (HBV). Most of the e Ag, Dane particles and DNA polymerase are retained in fraction III whereas the bulk of HBs Ag is recovered in fraction IV where only 22 nm spheres and short filaments are still identified. These results suggest that differences in quantitative distribution of HB virions together with alteration of infectious particles during the fractionation process may in addition to heat inactivation account for the relative hepatitis risk of the various plasma derivatives.
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PMID:Different fates of hepatitis B virus markers during plasma fractionation: a clue to the infectivity of blood derivatives. 67 42

A study was undertaken to establish markers for HBV replication in relation to HBeAg and anti-HBe. HBsAg carriers with serum HBeAg had DNA polymerase activity in the serum and HBcAg in the liver nuclei. Anti-HBe positive and anti-HBe/HBeAg negative sera lacked these markers. For anti-HBc the following geometrical mean titers were calculated: 1: 12,000 for HBeAg positive, 1:9, 100 for anti-HBe and anti-HBc positive, and 1:2,800 for anti-HBc positive anti-HBe/HBeAg negative asymptomatic HBsAg carriers. Follow up studies revealed mostly unchanged anti-HBc titers in all three groups over an observation period of ten to twenty months. Our data argue for a prolonged HBV replication in all HBsAg carrier subgroups compared to individuals with an uncomplicated acute virus-B-hepatitis. This study gives no final answer whether HBeAg negative HBsAg carriers have a continous HBV replication.
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PMID:Anti-HBc titers in HBeAg and anti-HBe positive asymptomatic HBsAg carriers. 67 25

We have studied prospectively 478 subjects exposed to hepatitis B virus and 20 pregnant women who developed HBs antigen during the last trimester of pregnancy. The results suggest that the DNA polymerase assay might be useful for the diagnosis of hepatitis B infection and that in confirmed cases of hepatitis, the enzyme might be detected in the absence of HBs antigen. HBe antigen appeared in 19% of those subjects who developed HBs and a positive correlation between HBe antigen and DNA polymerase was found in 40% of the cases positive for this antigen. The data presented also suggest that HBe antigenemia in pregnant women is not consistently associated with HBs infection in the babies born to them. However the children born to HBe positive mothers are at higher risk than those born to HBe negative mothers.
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PMID:Diagnosis of hepatitis B by Dane particle associated DNA polymerase assay. 73 Dec 23

A high positive correlation was found between e antigen (HBe Ag) and DNA polymerase in hemodialyzed patients with acute hepatitis B, chronic carriers of hepatitis B surface antigen undergoing hemodialysis, and patients with chronic hepatitis. In contrast, the correlation was poor in nonhemodialyzed patients with acute hepatitis. Among the patients with chronic hepatitis, HBe Ag and DNA polymerase were were found mostly in those with aggressive hepatitis and rarely in those with persistent hepatitis. This difference was significant (P less than 0.01) and suggests that the persistence of these antigens may be a factor in the progression of the disease. Our data also indicate that the development of antibodies to HBe Ag (anti-HBe) might be a sign of a favorable prognosis, since 50% of the patients with persistent hepatitis vs. 6% of the patients with aggressive hepatitis were anti-HBe-positive. Inhibitors of DNA polymerase, which are possibly antibodies, appeared regularly after acute hepatitis and were transient. Their presence may be associated with viral replication.
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PMID:e antigen and antibody, DNA polymerase, and inhibitors of DNA polymerase in acute and chronic hepatitis. 91 41

To determine the relation between the presence of donor DNA polymerase and e antigen, and recipient hepatitis, we tested, under code, serums from a controlled trial of hepatitis B immune globulin used to treat individuals accidentally inoculated with HBs Ag-positive blood. All recipients lacked antibody to HBs Ag. In 29 of 31 donors, both polymerase and e were in perfect agreement; both demonstrated a highly significant correlation with recipient hepatitis (P less than 0.001). DNA polymerase/e-negative blood did not cause hepatitis. Blood containing polymerase or e antigen did not cause hepatitis in six of 31 and four of 18 recipients, respectively. Hepatitis did not correlate with transaminase or duration of antigenemia in the donor. Polymerase and e appear to be indicators of the relative infectivity of HBs Ag-positive serum, particularly after small-volume exposure. They may be important determinants in assessing infectivity of chronic carriers of HBs Ag and in evaluating efficacy of hepatitis B immune globulin and hepatitis B vaccines.
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PMID:Type B hepatitis: the infectivity of blood positive for e antigen and DNA polymerase after accidental needlestick exposure. 96

In acute cases of hepatitis, DNA polymerase activity was found 2 to 3 times more frequently than positive radioimmunoassay. For each case the DNA polymerase reactivity was shown to be associated with hepatitis B antigens. Inhibitors to this DNA polymerase, with properties of IgM and IgG antibody, were found in 13 of 34 cases of acute hepatitis but only in 1 case out of 22 of cirrhosis. During the course of the acute disease these antibodies were detected 3 times more frequently than those to HBs antigen; the two types of antibodies were almost always found separately in different patients, those to DNA polymerase were apparently transient and developed earlier since they were found as early as 3 days after the clinical onset and no later than the 6th week following the onset.
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PMID:Comparison of DNA polymerase and radioimmune assays for the detection of hepatitis B antigens and antibodies. 120 57

The carbocyclic analog of 2'-deoxyguanosine (CdG) is active against herpes simplex virus (HSV), human cytomegalovirus, and human hepatitis-B virus. In order to understand the mechanism of action of this compound against HSV, we have evaluated (a) the incorporation of [3H]CdG into viral and host DNA in HEp-2 cells infected with HSV and (b) the interaction of the 5'-triphosphate of CdG (CdG-TP) with the HSV DNA polymerase and human DNA polymerases alpha, beta, and gamma (EC 2.7.7.7). Incubation of HSV-1-infected HEp-2 cells with [3H]CdG resulted in the incorporation of CdG into both the HSV and the host cell DNA. These results indicated that CdG-TP was used as a substrate for HSV DNA polymerase and for at least one of the cellular DNA polymerases. Degradation of both viral and host DNA with micrococcal nuclease and spleen phosphodiesterase indicated that CdG was incorporated primarily into internal positions in both DNAs. The viral DNA containing CdG sedimented in neutral and alkaline sucrose gradients in the same way as did viral DNA labeled with [3H]thymidine, indicating that the HSV DNA containing CdG was similar in size to untreated HSV DNA. CdG-TP was a competitive inhibitor of the incorporation of dGTP into DNA by the HSV DNA polymerase (Ki of 0.35 microM) and the human DNA polymerase alpha (Ki of 1 microM). CdG-TP was not a potent inhibitor of either DNA polymerase beta or gamma. Using DNA-sequencing technology, CdG-TP was found to be an efficient substrate for HSV DNA polymerase. Incorporation of CdG monophosphate (CdG-MP) into the DNA by HSV DNA polymerase did not interfere with subsequent chain extension. These results suggested that the antiviral activity of CdG was due to its incorporation into the DNA and subsequent disruption of viral functions. In contrast, CdG-TP was not as good as dGTP as a substrate for DNA synthesis by DNA polymerase alpha, and incorporation of CdG-MP by DNA polymerase alpha inhibited further DNA chain elongation.
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PMID:Incorporation of the carbocyclic analog of 2'-deoxyguanosine into the DNA of herpes simplex virus and of HEp-2 cells infected with herpes simplex virus. 131 7


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