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)

Seventeen out of 30 patients with chronic hepatitis type B with hepatitis B e antigen (HBeAg) in serum remained persistently positive for e antigen, while 13 seroconverted to antibody (anti-HBe) when followed over a period of one to five years. Initial levels of serum hepatitis B virus (HBV) markers, such as the hepatitis B surface antigen (HBsAg), HBeAg, and HBV-DNA polymerase (HBV-DNAP) were similar in the two groups of patients, while initial titres of the HBsAg-associated receptor for polymerized human serum albumin (pHSA), recently identified on HBV particles, were significantly higher in the patients who remained HBeAg positive (mean titre +/- SD = 2(-7.00) +/- 2(-3.2)) compared to the cases who eventually seroconverted to anti-HBe during the follow-up (2(-2.54) +/- 2(-2.14) P less than 0.001). A receptor titre above 1:64 by haemagglutination was highly predictive of persistence of HBeAg, suggesting that in patients with HBeAg-positive chronic hepatitis testing for the HBsAg-associated pHSA receptor may be useful in predicting the duration of HBe antigenaemia, with relevant clinical and prognostic implications.
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PMID:Virus receptors for polymerized human albumin: a prognostic marker in HBeAg-positive chronic hepatitis type B? 629 60

Several drugs which react with DNA decrease hepatitis B viral (HBV) DNA polymerase activity in vitro. Because such an alteration of viral replication, if produced in patients with hepatitis B surface antigen (HBsAg)-positive chronic hepatitis, may lead to elimination of viral infection, we conducted a controlled trial of the use of the intercalating agent, quinacrine hydrochloride, in treatment of HBsAg-positive chronic hepatitis. No patient converted from HBsAg positive to negative during the trial and no consistent effect on HBV DNA polymerase activity was noted. Following treatment, elevated transaminase values and alterations of HBV markers were observed in several patients. Fluctuations of transaminase values and HBV markers may reflect alterations in host immunity and viral replication. Quinacrine alone is ineffective in therapy of chronic HBV infection. Additional study with intercalating agents, perhaps in conjunction with other drugs, is suggested.
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PMID:Randomized controlled trial of quinacrine for the treatment of HBsAg-positive chronic hepatitis. 635 4

Sera from 588 woodchucks were assayed for woodchuck hepatitis virus (WHV) markers using hepatitis B virus (HBV) reagents which have cross-reactivity with WHV markers. Twenty per cent of these woodchucks, trapped in Delaware, Maryland and Pennsylvania, had WHsAg; 50% of these had DNA polymerase. There are areas of high and low endemicity within these states. Female woodchucks may have a higher incidence of WHV markers than do males. Woodchuck hepatitis surface antigen (WHsAg) and anti-WHc often occur together but less commonly than HBsAg and anti-HBc do in human HBV infection. Experimental infection of woodchucks with WHV produced a prolonged infection (up to 40 weeks). WHsAg and DNA polymerase appeared to be more reliable indicators of infectivity than anti-WHc, woodchuck hepatitis e antigen (WHeAg) or anti-WHe. WHeAg was not detected throughout this period of infection, while anti-WHe appeared late in two of three experimentally infected animals. Four male and four female woodchucks which developed primary hepatocellular carcinoma in captivity were analyzed for WHV markers throughout their period of confinement. Seven were WHsAg and anti-WHc positive when captured. The animal that was free of WHV markers on capture converted to the WHsAg and anti-WHc positive state prior to the development of primary hepatocellular carcinoma. One primary hepatocellular carcinoma animal produced WHeAg and none anti-WHs or anti-WHe.
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PMID:Woodchuck hepatitis virus: experimental infection and natural occurrence. 638 96

There are reports in the literature that infection with hepatitis A virus in hepatitis B carriers can result in resolution of the carrier state. In an attempt to induce clearance of the carrier state of hepatitis B virus in two persistently infected chimpanzees, the chimpanzees were infused with documented non-A, non-B infectious material. Biochemical and histopathological evidence of hepatitis was accompanied by the unique abnormalities of endoplasmic reticulum associated with non-A, non-B hepatitis in the chimpanzees. Elevation of alanine aminotransferase was accompanied by fourfold reduction in one chimpanzee and sixfold reduction in the other in the plasma levels of HBV-associated DNA polymerase activity and simultaneously by twofold reduction in the concentration of hepatitis B surface antigen in both chimpanzees. A mediator may account for these changes in markers of hepatitis B virus infection, and this mechanism may also explain the occurrence of spontaneous regression in some persistently infected carriers. The significance of transient red cell anaemia in non-A, non-B hepatitis, which was observed in one of the chimpanzees, is yet to be established.
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PMID:Non-A, non-B hepatitis in persistent carriers of hepatitis B virus. 640 22

A recently modified method using peroxidase labeled antibodies for light and electron microscopic demonstration of hepatitis B virus (HBV) was applied to the evaluation of hepatitis B surface antigen (HBsAg) on the surface of liver cells in biopsy specimens from 24HBsAg chronic carriers. Membranous distribution of HBsAg was demonstrated in diffuse or scattered hepatocytes in all 4 asymptomatic carriers and in 3 of the 20 patients with HBsAg-positive chronic active hepatitis or liver cirrhosis. In these patients with membranous expression of HBsAg, hepatitis B e antigen, Dane particles and DNA polymerase were often detected in sera, and large amounts of hepatitis B core antigen appeared in the liver. These results suggest that membrane-bound HBsAg may be expressed by the HBV genome. The ultrastructural study of liver cells showing membranous expression disclosed dense deposits of reaction product indicative of HBsAg on the cell membrane and/or on assembled particles within the extracellular space. In some hepatocytes showing both diffuse cytoplasmic and membranous expression of HBsAg, HBsAg-positive membrane of cisternae open to the intercellular space was connected with the liver cell membrane. These findings supported the conjecture that HBV associated antigens are integrated into the liver cell membrane.
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PMID:Immunoelectron microscopic observation of hepatitis B surface antigen on the surface of liver cells from patients with hepatitis B virus infection. 644 86

Abrupt increases of alanine transaminase were observed in 6 of 23 non-treated, male homosexuals with chronic hepatitis associated with hepatitis B virus. Before this occurrence, all subjects had hepatitis B e antigen (HBeAg) and elevated DNA polymerase activity. Within 3 months, HBeAg was nondetectable in 3 subjects and elevated DNA polymerase disappeared in 4. These serologic events were not always sustained, however. In 3 subjects, reactivation of hepatitis B virus infection occurred within the subsequent 6-month period. Serologic testing for cytomegalovirus, Epstein-Barr virus, delta agent, and hepatitis B surface antigen (HBsAg) subtype showed that episodes of clearance and reactivation were not explainable by secondary infection with these agents or infection with a different HBsAg subtype. Spontaneous clearance and reactivation of hepatitis B virus infection may commonly occur among male homosexuals with chronic type B hepatitis. These phenomena should be considered when evaluating the need for treatment or interpreting the results of investigations that use anti-viral therapy.
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PMID:Spontaneous clearance and reactivation of hepatitis B virus infection among male homosexuals with chronic type B hepatitis. 669 58

Two hepatitis B virus carrier chimpanzees which were superinfected with hepatitis A virus developed acute hepatitis followed by the production of antibodies to hepatitis A virus. The Southern blot technique employed to monitor liver hepatitis B virus DNA revealed that the amount of viral DNA in both animals was significantly reduced during the acute phase of hepatitis A infection. The levels of plasma hepatitis B DNA polymerase activity were also reduced in one chimpanzee. The high titers of HBsAg in the circulation remained unchanged throughout the study, and antibodies to the surface antigen and to e antigen were not detected. The morphological lesions in the liver were severe in one chimpanzee from whom one specimen showed both periportal focal necrosis and zonal parenchymal necrosis.
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PMID:Acute hepatitis A infection in hepatitis B chimpanzee carriers. 672 18

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

The hepatitis B virus infects only humans and higher apes. Viruses similar to the human hepatitis B virus (hepadna viruses) have been discovered in several nonprimate species including woodchucks, ground squirrels, and domesticated ducks. To search for other models of hepatitis B virus infection, we screened serum specimens from 64 exotic animals (24 species), 56 domesticated animals (6 species), and 52 laboratory animals (3 species). Samples were tested for deoxyribonucleic acid polymerase by enzymatic assay and for hepatitis B surface antigen and antibody and antibody to hepatitis B core antigen by radioimmunoassays. All sera were negative for deoxyribonucleic acid polymerase, hepatitis B surface antigen, and antibody to hepatis B core antigen suggesting that none of these animals harbored hepadna viruses in serum. However, 48% of the sera from 58% of the 33 species were reactive for antibody to hepatitis B surface antigen. This reactivity was blocked by human serum positive for hepatitis B surface antigen but not by control human serum. The antibody to hepatitis B surface antigen was generally present in low titer (95% were less than or equal to 1:16) and was often directed against subdeterminants of hepatitis B surface antigen (anti-d, anti-y, or anti-w). Characterization of the antibody to hepatitis B surface antigen by gel chromatography, sucrose density ultracentrifugation, affinity chromatography, and chemical inactivation suggested that it was entirely or predominantly immunoglobulin M antibody. Thus, many animals species have naturally occurring immunoglobulin M antibody to hepatitis B surface antigen detectable by radioimmunoassay. This antibody could arise as a result of either the intermittent spontaneous maturation of clones of antibody to hepatitis B surface antigen forming lymphocytes or exposure to environmental antigens that share epitopes with hepatitis B surface antigen. Similar naturally occurring antibody to hepatitis B surface antigen may be present in some humans.
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PMID:Antibody to hepatitis B surface antigen in nonprimate animal species. 684 Apr 76

Complete and defective hepatitis B virus (HBV) particles in sera and hepatocytes were observed by electron microscopy for an understanding of the maturation process of hepatitis B virus. To distinguish Dane particles with or without DNA on the basis of staining density with uranyl acetate, Dane particles, purified from sera of asymptomatic carriers, and Dane particle cores, separated by ultracentrifugation in a metrizamide density gradient, were observed by electron microscopy. Complete cores at a low density (1.19 to 1.23 gm/cm3) were electron dense and incomplete cores at a high density (1.23 to 1.27 gm/cm3) were partially electron dense or empty. These findings demonstrated that the presence or absence of DNA is reflected by the electron density of the core. Our result, in which less than 10% serum Dane particles have full cores in ultrathin sections of the pellet, is in agreement with Gerin's finding that defective Dane particles are predominent in sera. Naked core particles and Dane particles in two biopsy specimens from patients with hepatitis B surface antigen, hepatitis B e antigen, and DNA polymerase-positive, chronic active hepatitis were classified into complete versus incomplete particles on the basis of electron density. Nine hundred and fourteen naked core particles were detected in nuclei and cytosol of 68 hepatocytes. One hundred and five core particles (11.5%) were electron dense and 809 core particles (88.5%) were partially electron dense or empty. Furthermore, 488 Dane particles were observed in the cisternae of the endoplasmic reticulum of these hepatocytes. Fifty Dane particles (10.2%) had full cores, and 438 Dane particles (89.8%) had partially full or empty cores. These findings suggest that DNA may be incorporated into about 1 to 10% of core particles when they are assembled in nuclei of hepatocytes. Morphologic differences in damage to hepatocytes containing various frequencies of full Dane particles were also studied, but no significant correlation was found between damage in hepatocytes and frequency of full Dane particles.
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PMID:Full and empty particles of hepatitis B virus in hepatocytes from patients with HBsAg-positive chronic active hepatitis. 685 94


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