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)

Reactivity of monoclonal antibody (48-1), produced by the Epstein-Barr Virus (EBV) transformation method using lymphocytes from a chimpanzee infected with non-A, non-B hepatitis, on human liver biopsy specimens from 240 cases was studied. By means of indirect immunoperoxidase study (Secondary Antibody: Horseradish peroxidase labeled anti-human IgM.F(ab')2), the cases with non-A, non-B acute hepatitis showed a high positive reaction (15/24), while those cases with A-type and B-type hepatitis showed almost no reaction, suggesting that this 48-1 antibody strongly related to human non-A, non-B hepatitis. As for staining pattern, cytoplasms of some hepatocytes and large-size histiocytes were stained diffusely in pellet form, and were found scattered in each lobule. In addition, an EM study was made on positive cases using an immunoperoxidase method. However, a definite finding on peroxidase-reactive products was not obtained. We believe that this antibody (48-1) obtained by the EBV method would be useful in investigations of antigen-antibody systems related to non-A, non-B hepatitis.
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PMID:[Reactivity of 48-1 antibody with human liver tissue]. 283 Jun 52

By means of monoclonal antibodies against surface antigens of mononuclear cells we examined alterations of T-cell-subpopulations of peripheral blood and liver tissue in the course of acute HBsAg-negative hepatitis. Used methods for determination were the immunofluorescence for blood lymphocytes, respectively the peroxidase-anti-peroxidase-(PAP)-technique for round-cell-infiltrates of the liver based on paraffin fixed sections. The focus of attention was the relation of T4-(helper/inducer) to T8-(suppressor/cytotoxic) cells, the so-called immuno-regulatory quotient. With advancing improvement in the course of the disease we observed in peripheral blood a decrease of T4+/T8+ ratio from very high (3.6) to normal (1.9) values. By examination of the tissue round-cell-infiltrates we found a contrary behaviour to the peripheral blood with a low T4+/T8+ ratio in the liver, characteristic to more acute phases and due to an T8+-cell interchange between periphery and liver. This may be common for all virus diseases and without specificity for defined types of acute hepatitis. Beside this exists the possibility T4+/T8+ ratio has any prognostic value.
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PMID:[T cell subpopulations in peripheral blood and liver tissue in acute HBsAg-negative hepatitis]. 296 38

We have studied the effects of tunicamycin and inhibitors of the processing of N-linked glycans including N-methyl-1-deoxynojirimycin, castanospermine, mannodeoxynojirimycin, and swainsonine on the transport of glycoprotein E2 and the intracellular maturation of the coronavirus mouse hepatitis virus A59. Indirect immunofluorescence staining with monoclonal antibodies revealed that glycoprotein E2 exhibits different antigenic properties depending on the presence and on the structure of the N-linked oligosaccharides and that efficient transport of glycoprotein E2 to the plasma membrane requires the removal of glucose residues. In the presence of tunicamycin in the nonglycosylated E2 apoprotein was synthesized in normal amounts and readily acylated throughout the infectious cycle. This E2-species could not be detected on the surface of mouse hepatitis virus A59-infected cells with indirect immunofluorescence staining or lactoperoxidase labeling. N-Methyl-1-deoxynojirimycin and castanospermine, both of which selectively inhibited the processing glucosidases, caused a drop in virion formation by two log steps and a drastic delay in the surface expression of glycoprotein E2. The E2 species synthesized under such conditions was acylated but accumulated intracellularly in a compartment distinct from the Golgi. Concomitantly, synthesis of the matrix glycoprotein E1 of mouse hepatitis virus A59 was drastically impaired. Mannodeoxynojirimycin and swainsonine, which block later stages of the processing pathway, had less or no effect on the transport of glycoprotein E2 and the formation of virus particles.
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PMID:The effects of processing inhibitors of N-linked oligosaccharides on the intracellular migration of glycoprotein E2 of mouse hepatitis virus and the maturation of coronavirus particles. 299 42

Electron microscopic and virological studies of marmoset liver tissue with acute infection of hepatitis A virus (HAV), especially in the earlier stages of infection, were carried out to characterize the maturation process of HAV. Four marmosets were inoculated intravenously with HAV suspension and sacrificed 1 week, 2 weeks, 3 weeks and 4 weeks after inoculation respectively. Hepatitis A antigen (HAAg) in 10% liver homogenates of marmosets was examined by radioimmunoassay and a large amount of HAAg was detected in the liver homogenate of two marmosets sacrificed 2 weeks and 3 weeks after inoculation respectively. The histodiagnosis of the marmoset sacrificed 2 weeks after HAV inoculation was normal. However, many clusters of virus-like particles about 27 nm in diameter, in both "solid" and "empty" forms were found, mainly in vesicles of Kupffer cells by electron microscopy. In the animal that developed mild hepatitis 3 weeks after inoculation HAV-like particles were found in vesicles of hepatocytes by electron microscopy. By immune electron microscopy using peroxidase-conjugated anti-hepatitis A antibody, HAAg was detected on the particles present within the cytoplasmic vesicles of Kupffer cells or hepatocytes and on the surrounding membrane of the vesicles which contained HAV-like particles.
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PMID:Localization of hepatitis A virus in marmoset liver tissue during the acute phase of experimental infection. 300 96

The kinetics of delta antigen (HDAg) and anti-delta antibody (anti-HD) was analyzed in 22 acute delta hepatitis infections (11 coinfections and 11 superinfections), with an enzyme immunoassay developed by Organon Teknika and with two commercially available assays: Deltassay, a test for HDAg from Noctech and Abbott anti-delta enzyme immunoassay, a test for anti-HD from Abbott Laboratories. In seven cases, HDAg was detected with the Organon assay but not with Deltassay. These discrepancies were not related to the type of hepatitis delta virus infection. All samples from these patients taken beyond week 4 of illness were found anti-HD positive with both the Organon and Abbott anti-HD assays. These data reflect the lack of sensitivity of Deltassay. In no instance were HDAg and anti-HD present simultaneously when tested with the Organon assays. On the contrary, 10 sera among the 28 that were HDAg positive with the Organon assay also were found anti-HD positive with the Abbott test. We suspected that the test procedure recommended by Abbott (a one-step competitive assay) may have yielded false-positive anti-HD results when HDAg present in the sera reacted with peroxidase-labeled anti-HD of the kit. To determine the specificity of the simultaneous presence of HDAg and anti-HD, these 10 sera were retested with the Abbott anti-HD assay, but by a modified two-step procedure that avoided contact between sera and labeled antibody. For six sera a negative result was obtained with the second procedure, suggesting that a false anti-HD reaction occurred with the standard test procedure. For four sera a positive result with both procedures was indicative of the simultaneous presence of HDAg and anti-HD. In conclusion, assay for HDAg was found very convenient for the early diagnosis of acute hepatitis delta virus infections. Seroconversion to anti-HD could be used for a late diagnosis 2 to 5 weeks after the beginning of illness. However, anti-HD results obtained with one-step competitive assays have to be interpreted carefully in HDAg-positive sera.
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PMID:Kinetics of delta antigen and delta antibody in acute delta hepatitis: evaluation with different enzyme immunoassays. 304 50

Liver biopsy specimens from patients positive for serum HBsAg reveal various expression patterns when properly stained by immunohistochemical techniques for the demonstration of HBsAg, HBcAg and HDAg. A negative staining for these three antigens seems to be associated with two conditions, i.e., self-limiting acute lobular hepatitis (ALH) or low amounts of intrahepatic antigens. The discrepancy between serum positivity and tissue negativity for HBsAg can be explained either by sampling error or by the higher sensitivity of the radioimmunoassay as compared with immunohistochemical methods. The use of amplification systems such as the avidin-biotin-peroxidase complex enhances the sensitivity of immunohistochemical peroxidase-antiperoxidase (PAP) techniques and makes it possible to detect very small amounts of both HBsAg and HBcAg in liver cells from paraffin-embedded tissue sections which had been negative with the conventional PAP technique. In cases with a positive staining for viral antigens, two main expression patterns (non-aggressive and aggressive) can be distinguished. The non-aggressive pattern is reflected in the HBcAg-free HBsAg-positive type (HBsAg carrier) or the generalized type of nuclear core (HBcAg carrier), while the aggressive pattern is reflected in the presence of HDAg, the presence of HDAg and HBcAg, the focal type of nuclear core or the cytoplasmic HBcAg. Superinfection of HBsAg carriers or switching from generalized to focal core, with or without cytoplasmic expression of HBcAg, results in transition from non-aggressive to aggressive pattern. The aggressive pattern occurs in association with histological features of chronic active hepatitis (CAH). When it occurs in ALH cases or in milder forms of chronic hepatitis, an evolution into CAH has to be expected. Features of severe CAH, eventually with cirrhosis, are found in association with two new expression patterns: the cytoplasmic core and the simultaneous presence of HBcAg and HDAg. When features of CAH are observed in liver tissue specimens with HBcAg-free HBsAg-positive type, the liver disease may be due to viral superinfection or to non-viral etiology, e.g., alpha 1-antitrypsin deficiency.
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PMID:Immunohistochemical techniques for the demonstration of viral antigens in liver tissue. 306 47

For the purpose of diagnosing non-A, non-B hepatitis, an indirect immunoperoxidase method using the monoclonal antibody 48-1 was carried out. Human liver biopsy specimens of 74 cases with various hepatic diseases containing non-A, non-B hepatitis were investigated by using optical microscopy. Moreover, cases with non-A, non-B hepatitis were clinico-pathologically examined. Peroxidase-positive hepatocytes were found in 13 cases of the 74 cases. The thirteen cases were as follows; 8 cases with acute hepatitis (non-A, non-B type), 2 cases with chronic hepatitis (non-A, non-B type), 2 cases with acute hepatitis (B type), 1 case with chronic hepatitis (B type). The frequency of positive peroxidase staining was high (80%) in acute hepatitis (non-A, non-B type), but it was not significant statistically. On histological examination, acidophilic condensation was frequently seen in liver specimens of cases with acute hepatitis (non-A, non-B type). Furthermore, the correlation between acidophilic condensation and peroxidase positive staining was statistically seen. It is suggested that the peroxidase staining by using monoclonal antibody 48-1 is useful for diagnosis of acute hepatitis (non-A, non-B type).
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PMID:[Indirect immunoperoxidase method using a monoclonal antibody and clinico-pathological examination of non-A, non-B hepatitis]. 314 Mar 42

An enzyme-linked immunosorbent assay (ELISA) was developed which permits the assay of specific secretory immunoglobulin A (sIgA) antibodies against hepatitis B surface antigen (HBsAg) in saliva. The assay is based on the binding of sIgA antibodies present in saliva to microtitre plates coated with excess of F(ab')2 anti-secretory component antibodies, followed by the addition of specific antigen, HBsAg and finally peroxidase-labelled anti-HBsAg. The assay is fast, simple, reproducible and antigen specific as shown by total absence of inhibition of specific antigen by unrelated antigens but significant inhibition of labelled anti-HBsAg by unlabelled anti-HBsAg. The values obtained for hospital personnel exposed to hepatitis infections (0.068 +/- 0.083 U/ml) and for post-icteric hepatitis B patients (0.062 +/- 0.033 U/ml) were significantly higher than values in control subjects (0.013 +/- 0.006 U/ml).
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PMID:An 'antigen capture' ELISA for secretory immunoglobulin A antibodies to hepatitis B surface antigen in human saliva. 318 91

Liver biopsy specimens from 58 American patients with chronic type B hepatitis were investigated for the presence and distribution of the hepatitis B core (HBcAg) and surface (HBsAg) antigens by peroxidase-anti-peroxidase techniques. HBsAg was detected in 43 (77%) and HBcAg in 52 (90%) patients. HBcAg was present in 50 of 51 (98%) patients with hepatitis B e antigen (HBeAg) but in only two of seven (29%) of patients with antibody to HBeAg (anti-HBe). There was no correlation between severity of hepatitis or height of aminotransferase activities and the amount of HBsAg or HBcAg in hepatocytes but there was a positive correlation between amount of HBcAg and height of HBV-DNA and DNA polymerase activity in serum. Follow-up liver biopsies, taken 1 to 3 yr later, were available from 39 patients. HBcAg remained detectable in 25 of 26 patients with persistence of HBeAg but disappeared in 12 patients who had lost HBeAg. In nine patients, HBcAg was cytoplasmic as well as nuclear in distribution. Seven of these patients had an intense lobular hepatitis with marked elevations in aminotransferase activities. These findings indicate that the amount of HBcAg in liver correlates with the amount of serum hepatitis B virus as quantified by serum levels of DNA polymerase and HBV-DNA. The amount of nuclear HBcAg does not correlate with the severity of the liver disease, but the presence of cytoplasmic HBcAg usually reflects an active and severe ongoing hepatitis.
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PMID:Peroxidase-anti-peroxidase detection of hepatitis B surface and core antigen in liver biopsy specimens from patients with chronic type B hepatitis. 332 17

The biopsied kidneys from three patients with hepatitis Be antigen (HBeAg)-associated nephropathy were observed by light microscopy, immunohistochemistry and electron microscopy. By an indirect technique utilizing horseradish peroxidase-conjugated antisera, HBeAg was found to be deposited in a diffuse granular fashion along the glomerular capillary wall. No deposition of hepatitis Bs or hepatitis Bc antigen was detected. The three cases were diagnosed as HBeAg-associated nephropathy. Ultrastructurally, there were finely granular electron-dense deposits in the subendothelial area, basement membrane, mesangial area and subepithelial area of the glomerular tufts. In all three cases, virus-like particles between 30 and 70 nm in diameter were also found in such areas of the glomerular tufts, and rarely in the glomerular capillary lumen and space of Bowman. They occasionally formed clusters in the phagosomes of mesangial cells. In addition, tubulo-reticular structures were noted in the cytoplasm of endothelial cells in the glomerular capillaries. The presence of HBeAg both in the serum and in the kidney and of virus-like particles in the glomerular tufts suggests that HBeAg is causally related to the development of HBeAg-associated nephropathy.
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PMID:Ultrastructure of kidney from three patients with HBeAg-associated nephropathy with special reference to virus-like particles in the glomerular tufts. 339 23


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