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 infants, born to mothers with hepatitis B virus infection, were inoculated within 7 days of birth with immune serum globulin containing antibody to hepatitis B surface antigen (HBsAg) titers of 1:32 to 1:64 as measured by passive hemagglutination. Six of nine infants (66.7%) born to HBsAg-positive carrier mothers became HBsAg-positive within 3 mo of age. In addition, two of three treated infants born to mothers with acute hepatitis B during the delivery period also developed HBsAg. The hepatitis e antigen was detected in four of five carrier mothers and in two mothers with acute hepatitis, whose infants subsequently became HBsAg positive. In addition, hepatitis B-specific DNA polymerase activity was detected in the seven HBsAg-positive mothers who transmitted the virus to their infants. All eight infants have remained persistently HBsAg positive. Thus, the immune serum globulin containing low-titer antibody to HBsAg is not protective when given to infants born to HBsAg carrier mothers or to mothers with acute hepatitis B during the delivery period.
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PMID:Failure of immune serum globulin to prevent hepatitis B virus infection in infants born to HBsAg-positive mothers. 8 62

Serum levels of hepatitis B virus specific DNA polymerase and hepatitis B e antigen were studied serially in 34 patients with hepatitis B virus infection--20 who had the acute illness and recovered, seven who died with fulminant disease, three who died as a result of subacute hepatic necrosis, and four who went on to develop chronic active hepatitis. DNA polymerase activity was present in 16 (80%) and HBeAg in 13 (65%) of the uncomplicated cases at presentation and in all of those patients from whom the initial sample was obtained before the peak in aminotransferase. Both markers disappeared after 30 days from the onset but DNAP remained persistently positive during a follow-up period of four to 10 months in the four patients who progressed to chronic hepatitis. These results indicate that DNAP and HBeAg are transiently present in all cases of acute hepatitis B. Only their persistence after the acute episode could represent a useful prognostic marker of chronically. In this respect, DNAP was more reliable in our patients than HBeAg. In uncomplicated acute hepatitis, the peak in DNAP levels, which defines the time of maximum virus replication in the liver, preceded the peak in aminotransferase levels. Among the 10 patients who developed massive liver damage after hepatitis B infection, DNAP was detected in five of the seven with fluminant hepatitis, with enzyme levels that were comparable with those observed in uncomplicated acute hepatitis and presentation, but not in the cases of subacute hepatic necrosis. These findings are consistent with the hypothesis that in hepatitis B infection, liver damage, whatever the severity, is not directly related to the degree of virus replication.
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PMID:Changes in hepatitis B virus DNA polymerase in relation to the outcome of acute hepatitis type B. 43 51

In a study of the distribution of e-antigen and anti-e in subjects whose blood was positive for hepatitis B surface antigen (HBsAg), patients with acute hepatitis B who were tested during the incubation period were all e-antigen-positive but after the onset of illness e-antigen was detected in only 11%. Persistence, and in some instances reappearance of e-antigen in those who became long-term carriers of HBsAg was associated with high titres of HBsAg. There was a high incidence of e-antigen in those conditions in which cell-mediated immunity may be depressed, including Down's syndrome and chronic renal failure. The majority of HBsAg carries identified as sources of infection were e-antigen-positive. A postive reaction for e-antigen is evidently associated with a defective immune response to hepatitis B virus infection which permits continued replication of virus in liver cells accompanied by high titres of HBsAg, numerous Dane particles and detectable DNA polymerase in the blood with consequently a greater likelihood of transmitting infection. Although it cannot be assumed that anti-e positive carriers of HBsAg are not infective, it may be necessary, in the assessment of passive or active immunization for the control of hepatitis B, to take into account the e-antigen/antibody status of possible sources of infection.
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PMID:e-Antigen: a link between immune response and infectivity in hepatitis B? 73 Oct 22

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

Sera from patients with acute hepatitis, cirrhosis or chronic hepatitis, as well as sera from healthy carriers and controls were examined for HBS antigen, DNA polymerase activity and for antibodies to HBS, HBC and DNA polymerase. The data presented suggest that in acute hepatitis the DNA polymerase test enabled us to diagnose at least 20% more cases of hepatitis B than with the RIA but that the DNA polymerase test is of little value for the screening of blood donors since all the healthy carriers gave negative results. As concerns the antibodies to DNA polymerase they appeared in at least 50% of the patients with acute hepatitis, they were transient and only detectable at the early beginning of the disease. These antibodies were also found to be different from the anti-HBS and anti-HBC antibodies.
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PMID:Transient antibodies to DNA polymerase in acute hepatitis B and related diseases. 96 84

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 aim of the study was to test the clinical value of HBV DNA polymerase (DNAp) determination in patients with various forms of HBV infection, namely: acute hepatitis, chronic hepatitis, cirrhosis and healthy HBV carriers. The determination of DNAp was found to be particularly useful in patients with chronic HBV infection with active virus replication (HBeAg+) independent of histopathological changes.
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PMID:[Hepatitis B virus DNA polymerase activity in various clinical forms of HBV infection]. 140 93

Since 1965, when Blumberg discovered the Australia antigen, the hepatitis B surface antigen (HBsAg), the research on viral hepatitis has rapidly progressed. The identification of specific hepatitis B associated antigens and antibodies in blood, and liver tissue, together with the improvement of detection systems, have enhanced our knowledge about the mechanism of liver injury and the natural history of hepatitis B virus (HBV) infection. Now it has been recognized that HBV has no direct cytopathic effect on hepatocytes and that hepatocyte necrosis is associated with the virus induced immunological reaction of the host. From the reaction, there are two types of HBV infection, i.e., transient (acute) and persistent (chronic) infection. In addition to the conventional measurements, such as HBsAg, anti-HBs, anti-HBc, HBeAg, anti-HBe and anti-IgM HBc, recently pre S1, pre S2 antigen/antibody systems and polymerized human albumin receptor and antibody have been developed. The significance of the detection of these antigen/antibody systems was discussed. On the other hand, to determine the presence of HBV, the state of HBV replication or the infectivity directly, HBV associated DNA polymerase and HBVDNA should have been detected. (Very recently, the polymerase chain reaction method has been introduced to detect very small amounts of HBVDNA). In this presentation, the change of these viral markers in various cases was shown, and especially emphasized was anti-IgM HBc in acute hepatitis and HBeAg/Ab status in chronic liver disease. Lastly, the present state of Interferon therapy for type B chronic hepatitis was mentioned.
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PMID:[Diagnosis of type B hepatitis]. 219 6

Sera from four patients with acute hepatitis B and 87 patients with chronic hepatitis B were examined quantitatively for pre-S1 and pre-S2 antigens by solid-phase enzyme immunoassays. Pre-S1 and pre-S2 antigens were detected in HBsAg-positive sera irrespective of the presence of viral replicative markers, and their titers correlated with those of HBsAg (r = 0.74, p less than 0.01; r = 0.74, p less than 0.01, respectively). Sera positive for HBeAg showed higher titers of pre-S1 (p less than 0.01) and pre-S2 (p less than 0.01) antigens than sera negative for HBeAg. The titers of pre-S1 and pre-S2 antigens also correlated with the levels of HBV-associated DNA polymerase activity (r = 0.51, p less than 0.01; r = 0.59, p less than 0.01, respectively) and HBV-DNA (r = 0.50, p less than 0.01; r = 0.46, p less than 0.01, respectively). However, the ratios between the titers of pre-S antigens and HBsAg had no significant relationships with those viral replicative markers. These findings suggest that the expression of pre-S antigens is intimately related to the expression of HBsAg and that they are not useful as markers of viral replication. The ratios between the titers of pre-S antigens and HBsAg tended to be high in patients with chronic active hepatitis and high aminotransferase levels. This finding may have been due to the hepatic release of pre-S antigens, over-production of which may have some relationship to liver injury.
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PMID:Quantitative analysis of pre-S1 and pre-S2 in relation to HBsAg expression. 229 69

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


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