Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Liver biopsies from 12 patients with chronic Non-A, Non-B (NANB) hepatitis, 7 with hepatitis B surface antigen (HBsAg) positive chronic liver disease, 1 HBsAg positive normal carrier, and 4 patients with non-viral liver disease, were examined by electron microscopy for cytoplasmic and nuclear changes. Aggregates of particles measuring 20-35 nm in diameter were noted in the nuclei of 8 of 12 patients with NANB chronic hepatitis, but not in the other groups. The tubular changes seen in the endoplasmic reticulum (ER) of chimpanzees with NANB hepatitis were not noted in biopsies from any of our patients.
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PMID:Ultrastructural features in chronic non-A, non-B (NANB) hepatitis: A controlled blind study. 680 Nov 96

A new ultrastructural cytoplasmic marker designated as type 2, and distinct from type 1 previously associated with NA-NB hepatitis in chimpanzees, was found in hepatocytes of two patients and of one experimentally infected chimpanzee. These cases represent a minority of all cases we studied as presumed NA-NB viral hepatitis. Type 2 marker consists of tubular structures composed of an assembly of ring-like units coated with smaller uniform fragments, accumulated in different patterns in dilated cisternae of the endoplasmic reticulum. Preliminary data using immunofluorescence with NA-NB hepatitis convalescent serum and antiserum against fibrinogen are reported. Type 2 marker may represent a different agent or a different reaction pattern to one agent of NA-NB viral hepatitis. Its features are compared with those of hepatitis B.
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PMID:New ultrastructural marker in hepatocytes in non-A, non-B viral hepatitis. 681 11

A seroimmunologic evaluation of 57 children with chronic hepatitis is presented. Twenty-one patients had chronic persistent hepatitis and 36 had chronic active hepatitis. Serum samples obtained before treatment were tested for HBsAg, anti-HBs, anti-HBc, smooth muscle antibody, and antibody to endoplasmic reticulum. A persistently positive HBsAg was observed in the serum of 18 of the 21 patients with chronic persistent hepatitis. The chronic active hepatitis group was divided into three subgroups according to the presence of hepatitis B-virus markers (7 patients), smooth muscle antibody (10 patients), and endoplasmic reticulum antibody (9 patients). Determination of these markers could be useful for classifying children with chronic hepatitis.
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PMID:Seroimmunologic classification of chronic hepatitis in 57 children. 684 Jun 86

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

A close correlation between the presence of hepatitis B surface antigen and albumin in the cytoplasm of hepatocytes infected with hepatitis B virus was established by immunofluorescence and immunoelectron microscopy in 52 liver biopsy specimens of various forms of hepatitis and liver cirrhosis. Albumin deposits usually accompanied cytoplasmic content of hepatitis B surface antigen, but were less frequently observed together with hepatitis B antigen localized in or on the membranes. Ultrastructural observations demonstrated albumin on the tubular and spherical forms of hepatitis B surface antigen in the endoplasmic reticulum. The hepatocytes with the content of hepatitis B surface antigen and albumin showed the ability of binding with the fluorescein-labeled preparation of polymerized human serum albumin. The affinity of polymerized albumin to hepatitis B surface antigen was considerably increased after preincubuation of liver sections with 2-mercaptoethanol that removed most of the originally present albumin. This may be indicative for the role of disulfide bonds in the formation of hepatitis B surface antigen-albumin complexes. These results justify the hypothesis that albumin may be incorporated into the viral coat protein during its synthesis in the cytoplasm of infected hepatocytes.
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PMID:Hepatitis B surface antigen and albumin in human hepatocytes. An immunofluorescent and immunoelectron microscopic study. 700 3

A prospective series of 45 liver biopsies taken from 22 renal transplant patients was investigated for the presence of hepatitis B antigen core (HBc) and surface (HBs) components by electron microscopy. At the time of each biopsy serum HBs Ag was sought by radioimmunoassay. Sections were taken for the detection of HBs Ag by immunofluorescence. In seropositive patients, intravesicular tubular structures resembling HBs Ag were found in 61% of biopsies while the intranuclear core HBc was present in 69%. No correlation could be made between the ultrastructural pattern of the viral components and the intensity of the histological liver damage. During the follow up, there was an accumulation of both HBs and HBc Ag even in a period as short as 1 year. The 9 liver specimens examined after three years of transplantation showed a marked accumulation of both antigens. Thus the expression of HB Ag at the hepatocellular level seems to correlate better with the duration of antigenaemia than with the histological pattern. Lastly, on matched semithin and ultrathin sections, the ground glass appearance of cytoplasm appeared to correlate with smooth endoplasmic reticulum distorsion, irrespective of the simultaneous presence or absence of intravesicular tubular structures. The sanded nuclei expressed a rare massive accumulation of core antigen.
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PMID:Hepatocyte localization of hepatitis B core and surface antigens in renal transplant recipients. An ultrastructural prospective study. 701 55

The site of Dane particle formation in hepatocytes was studied by routine electron and immunoelectron microscopy of liver biopsy specimens from 10 patients with hepatitis B e antigen-positive chronic active hepatitis. With routine electron microscopy, core particles were abundant in cytosol, often adjacent to the cell membrane, and occasionally in the microvilli. Figures suggestive of budding of endoplasmic reticulum with a core particle into the cisternae of endoplasmic reticulum were observed frequently. There were also figures suggestive of direct budding with a core particle from the surface of the cell. With the immunoelectron microscopy, the core particles were found to be positive for hepatitis B core antigen and the endoplasmic reticulum and the plasma membrane were positive for hepatitis B surface antigen. These findings suggest that the most plausible mode of formation of the Dane particle is by budding of hepatitis B surface antigen-positive endoplasmic reticulum membrane into the cisternae. In addition, formation of the Dane particle may also take place at the surface of the hepatocyte by a similar mechanism.
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PMID:Electron and immunoelectron microscopic study of Dane particle formation in chronic hepatitis B virus infection. 708 14

Electron microscopic observations in 30 cases of HBsAg positive liver disease and 12 asymptomatic carriers of HBsAg suggested the following mechanism of intracellular development of Dane particles: core particles migrated from the nucleus into the cytoplasm through the nuclear pores. Intracytoplasmic core particles protruded into the cisternae of endoplasmic reticulum by budding the outer coat of Dane particles being derived from the membrane of endoplasmic reticulum. Release of Dane particles into the blood stream by reversed pinocytosis was suggested by the finding of submembranous localization of endoplasmic reticulum containing these particles. No budding from the cell surface of the hepatocytes was encountered. Dane particles in the hepatocytes were detected in 14 of 15 cases positive for serum HBeAg while no particles were seen in 27 HBeAg negative cases, thus suggesting that serum HBeAg reflected ongoing replication of hepatitis B virus in the hepatocytes.
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PMID:Electron microscopic studies of Dane particles in hepatocytes with special reference to intracellular development of Dane particles and their relation with HBeAg in serum. 730 84

Liver-membrane auto-antibodies (LMA) were searched for in children with histologically proven chronic active hepatitis. LMA were found in the serum of all 20 patients under study. In the 6 cases associated with hepatitis B virus, LMA were the sole marker for auto-immunity; in 11 cases, negative for HBsAg, other anti-tissue antibodies, smooth muscle or endoplasmic reticulum antibody, coexisted. Neither prior to therapy nor during treatment with prednisone and azathioprine was there any correlation between titres of LMA and those of other auto-antibodies nor with the assessment of histological activity. Although a reliable diagnostic marker, LMA, as revealed by using heterologous hepatocytes, appear to convey limited values as a prognostic marker of chronic active hepatitis in children.
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PMID:[Autoantibodies to liver membrane in children with chronic active hepatitis (author's transl)]. 744 13

The large hepatitis B virus (HBV) surface protein (L) forms two isomers which display their N-terminal pre-S domain at the internal and external side of the viral envelope, respectively. The external pre-S domain has been implicated in binding to a virus receptor. To investigate functions of the internal pre-S domain, a secretion signal sequence was fused to the N terminus of L (sigL), causing exclusive expression of external pre-S domains. A fusion construct with a nonfunctional signal (s25L), which corresponds in its primary sequence to sigL cleaved by signal peptidase, was used as a control. SigL was N glycosylated in transfected COS cells at both potential sites in pre-S in contrast to s25L or wild-type L, confirming the expected transmembrane topologies of sigL and s25L. Phenotypic characterization revealed the following points. (i) SigL lost the inhibitory effect of L or s25L on secretion of subviral hepatitis B surface antigen particles, suggesting that the retention signal mapped to the N terminus of L is recognized in the cytosol and not in the lumen of the endoplasmic reticulum. (ii) SigL was secreted into the culture medium even in the absence of the major HBV surface protein (S), while release of an L mutant lacking the retention signal was still dependent on S coexpression. (iii) s25L but not sigL could complement an L-negative HBV genome defective for virion secretion in cotransfections. This suggests that the cytosolic pre-S domain, like a matrix protein, is involved in the interaction of the viral envelope with preformed cytosolic nucleocapsids during virion assembly.
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PMID:Functions of the internal pre-S domain of the large surface protein in hepatitis B virus particle morphogenesis. 747 74


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