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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several animal and human demyelinating diseases of the central nervous system (CNS) are associated with RNA or DNA viruses. These viruses infect CNS cells lytically or persistently. They mainly belong to the group of envelope viruses which derive their envelope partly from the host cell membrane. The process of virus release may result in the appearance of new antigens of virus-infected cells or the incorporation of cell membrane material into the viral envelope. These changes may lead to an immune response which selectively injures the CNS. These alterations of host cell membranes and host cell functions, together with the immune mechanism, are central to many of the hypotheses regarding virus-induced demyelination. The role of virus infection in progressive multifocal leukoencephalopathy, subacute sclerosing panencephalitis, visna and mouse hepatitis virus infections, is discussed in relation to the demyelinating process of these diseases.
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PMID:Virus infection in demyelinating diseases. 21 25

Histologic study of eyes used as donor material for corneal transplant revealed one instance of massive leukemic infiltration with leukemic keratic precipitates on the fellow eye. In another eye, microabscesses composed of acute and chronic inflammatory cells containing Crytococcus neoformans were present. In a third patient metastatic anaplastic cells were present in the choroid. We think donor eyes are absolutely unacceptable if death was caused by any chronic neurologic disorder, unless clearly secondary to trauma. Eyes from patients with septecimia, hepatitis, jaundice and any evidence of any active viral infection, syphilis, and positive serology are also unacceptable. Extreme caution should be used in selecting eyes of patients with ocular or systemic malignancy, long-term diseases, particularly if immunosuppressive agents were used, where a history of eye disease exists, including corneal disease or dystrophy, iritis, absolute glaucoma or acute glaucoma, and eyes with a history of previous intraocular surgery.
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PMID:Corneal donor material selection. 21 75

The serologic and tissue markers of hepatitis B virus (HBV) were studied in 50 patients in whom hepatocellular carcinoma (HCC) was confirmed at autopsy. Serologic and tissue markers included serum hepatitis B surface antigen (HBsAg), tissue HBsAg, tissue hepatitis core antigen (HBcAg), and serum antibody to HBcAg (anti-HBc). Twenty-two patients had HCC arising in alcoholic cirrhosis; 2 of the 22 (9.1%) had one or more of the HBV tissue and serologic markers. This infection rate is similar to the rate of 7.9% observed in 63 control alcoholic cirrhotic patients without HCC. In contrast, 15 of 20 (75.0%) patients with HCC in nonalcoholic chronic active liver disease showed evidence of active HBV infection. One of 8 patients with HCC in normal liver had serum HBV markers. This result indicates that there is an extremely high prevalence of HBV infection among HCC patients with nonalcoholic chronic liver disease in the U.S.A. The prevalence of HBV infection in these patients is as high as that observed in Asia and Africa. Thus, it can be concluded that the lower prevalence rate of active HBV infection in HCC patients in the U.S.A. is the result of statistical dilution of HCC-B-viral disease by the large numbers of the alcoholic cirrhotic patients with HCC, and that if chronic active hepatitis type B were as common in the United States as it is in Africa and Asia, the frequency of occurrence of HCC might also be as high.
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PMID:Hepatocellular carcinoma in the U.S.A., etiologic considerations. Localization of hepatitis B antigens. 21 88

All human, simian, bovine and avian adenovirus types tested so far and the canine hepatitis virus induce interferon production in chick cells. This finding indicated this property to be characteristic for viruses belonging to the adenovirus group. Trypsin treatment, which had no effect upon the infectivity, diminished or eliminated the interferon-inducing abilities of crude adenoviruses, and thus the need for a trypsin-sensitive protein in interferon induction was suggested. T antigen and interferon were formed simultaneously in chick embryo fibroblast cells infected with human adenovirus type 12, and therefore the adenovirus-specific T antigen was resistant to the action of endogenous interferon synthetized by the same cells. In chicks inoculated with human types, the appearance of interferon was biphasic: an 'early' and a 'late' interferon could be demonstrated with maximum titre 4 and 10 hr, respectively, after virus infection. In chicks infected with adenoviruses, first interferon production and then a decreased primary immune response to sheep red blood cells was observed. It was assumed that in adenovirus-infected chicks the interferon produced by viral stimulus resulted in a transient immunosuppression.
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PMID:Interferon induction by adenoviruses. 22 39

Aleutian disease is a chronic persistent viral infection of mink characterized by hypergammaglobulinema, generalized plasmacytosis, sclerosing glomerulonephritis, polyarteritis, and plasma cell hepatitis with bile duct proliferation. The development of hepatic lesions was studied both light- and electron-microscopically in mink experimentally infected with Aleutian disease virus. Fifteen normal and 99 mink experimentally infected with Aleutian disease virus were used. Experimental mink were killed in intervals from 3 weeks to 23 months after infection, and liver sections were processed for both light- and electron-microscopic studies. Experimentally infected mink developed portal and intralobular lymphocytic and plasmacytic infiltrates in the liver 3 weeks after infection. Four to five weeks after infection there was evidence of early bile duct proliferation that began as an outgrowth of the portal bile ducts. Three to five months after infection a marked bile duct proliferation was present in some of the portal triads and adjacent liver lobules; but there was no tendency of these lesions to progress into biliary cirrhosis. Ultrastructural characteristics of proliferating bile duct cells were marked deformation, formation of multiple cell layers, reduction in the number of microvilli and desmosomes, and infiltration of the epithelial cells by lymphoid cells and plasmacytes. The hepatic lesions either develop by direct virus stimulation or by the deposition of virus-antibody complexes.
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PMID:[Pathogenesis of aleutian mink disease. VII. Chronic hepatitis with bile duct proliferation]. 24 13

Recent evidence indicates that viral hepatitis is sometimes associated with the production of extrahepatic tissue injury. Hepatitis B virus (HBV) infection is most commonly incriminated but non-type B hepatitis may also be involved. Three types of syndromes have been recognized. First, a serum sickness-like prodrome consisting of skin eruptions, urticaria and polyarthralgias or arthritis may occur from one to six weeks prior to the onset of hepatitis in 15 to 20 per cent of patients and usually disappears by the time the patient becomes jaundiced. There is extensive evidence that circulating immune complexes are responsible for these symptoms. Second, about 30 to 40 per cent of patients with typical polyarteritis nodosa have persistent hepatitis B surface antigenemia (HBs Ag). Circulating immune complexes composed of HBs Ag, antibody, and complement have been demonstrated together with deposits of immune complexes at sites of vascular injury. Third, an immune complex type of glomerulonephritis may occur following hepatitis B virus infection, usually in association with chronic active hepatitis. Thus there is impressive evidence that hepatitis viruses, especially HBV, may produce a variety of extrahepatic manifestations in which the mechanism of pathogenesis involves an immunologic process rather than direct viral invasion and cytopathogenicity.
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PMID:Extrahepatic manifestations of viral hepatitis. 24 19

Papular acrodermatitis of childhood (PAC) is characterized by papular eruption of skin, lymphadenopathy, and acute hepatitis B surface antigen (HBsAg)-positive anicteric hepatitis. To study the course of hepatitis B virus infection we followed 16 patients with PAC, 2 to 7 years of age, for periods ranging from 6 to 46 months. All patients tested developed hepatitis B surface antigenemia subtype ay, and produced antibody to hepatitis B core antigen with the highest incidence after 3 to 5 months. Half of the children investigated developed antibody to hepatitis B surface antigen 4 to 18 months (mean, 6.5) after the onset of PAC. At the end of the investigation, 31% of the children were still HBsAg-positive, 50% were antibody to hepatitis B core antigen-positive, and in 43% the activity of serum aminotransferases was abnormal. Liver biopsy repeated in 2 children showed chronic aggressive hepatitis. The pattern of antibody response to hepatitis B virus is similar in both HBsAg-positive hepatitis and PAC. The frequent development of HBSAg carrier state and the high proportion of children with liver abnormalities at the end of the investigation suggest an impaired clearance of hepatitis B virus and a tendency to chronicity.
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PMID:Immune response to hepatitis B virus in children with papular acrodermatitis. 33 78

Circulating immune complexes were measured by a radioimmunoassay specific for HB complexes in different clinical situations related to hepatitis B virus infection. The leukocyte migration inhibition test (LMIT) was performed simultaneously. Comparison with the clinical situation suggests that immune complexes are not responsible for the lesions, but that these lesions might be produced by the immunity demonstrated by the LMIT. A deficiency of this immunity is responsible for the persistence of infection. However, in chronic active hepatitis, LMIT is as deficient as in carriers and in this form of hepatitis the frequency and quantity of complexes are the highest: it is thus possible that in this case the lesions are nevertheless produced by the complexes.
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PMID:[Comparison between the presence of specific circulating immune complexes and the leukocyte migration inhibition test in different clinical forms of hepatitis B]. 33 69

Single liver biopsies from 102 clinically diagnosed hepatitis patients were examined by immunofluorescence for the presence of hepatitis B surface antigen (HBsAg) and hepatitis B core antigen (HBcAg), complement and immunoglobulin deposition, and for their capacity to fix human complement in vitro. Of the sixty-five HBsAg positive livers, fifty-three were histologically diagnosed as chronic hepatitis, three as acute hepatitis, five as acute hepatitis with signs of transition to chronicity, and four as 'near normal liver'. In the group with chronic hepatitis, HGcAg was observed in thirty-nine livers, all of which also had HBsAg. Thirty-five of these thirty-nine cases also had the ability to fix complement in vitro in the hepatocyte nuclei and/or cytoplasm. Of these thirty-five cases, twenty-nine were positive for immunoglobulin deposition on the nuclei. All of these cases had antibody to HBcAg in the blood, but only five had anti-HBs. The frequency of in vitro complement fixation and immunoglobulin deposition was higher in active forms of the disease, such as chronic aggressive hepatitis and active cirrhosis, than in non-active disease such as chronic persistent hepatitis and mild cirrhosis. By the application of double fluorescent staining techniques, complement fixation was observed in some HBcAg-positive nuclei. In the 'near normal liver' cases there was no intrahepatic accumulation of HBcAg, and despite the presence of anti-HBc in the blood, in vitro complement fixation and immunoglobulin deposition were both absent. The group of three HBsAg ositive 'acute hepatitis with signs of transition to chronicity' cases behaved similarly to those with chronic aggressive hepatitis and had circulating anti-HBc, in vitro complement fixation and immunoglobulin deposition in the hepatocytes. None had circulating anti-HBs. In the group sith HBs-positive acute hepatitis, anti-HGc in the blood was the only other evidence of hepatitis B virus infection.
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PMID:Hepatitis B core antigen immune complexes in the liver of hepatitis B patients. 38 86

The discovery of Australian antigen (HBsAg) has led to an increasing deal of knowledges about the virus of type B hepatitis (HBV); several markers of HBV have been detected and are becoming disposable for clinical and epidemiological purposes. The HBsAg is carried by 3 types of particulate structures discovered by electron microscopy as small spherical particles having diameter around 22 nm, long filaments and spherical particles having an overall diameter of the 42 nm (Dane-particle) with an electron-dense core. Dane-particle core contains circular double-stranded DNA molecules and an enzyme, the DNA polymerase. At present, Dane-particle is thought to represent the HBV, having properties consistent with those of a complete virus. Four antigen/antibody systems related to viral type B hepatitis have been discovered; they have been designated with the following nomenclature: HBsAg/anti-HBs, HBcAg/anti-HBc, HBeAg/anti-HBe, epilon antigen/anti epilson. The availability of the HBV markers for clinical purposes will permit a better understanding of the sequence of the biological reactions as well as of the clinical and epidemiological features concerning this viral infection: incubation period, acute disease, resolution, chronic carrier state, actively or passively immunized subject, persistent or subsided infectivity, prognosis.
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PMID:[Markers of type B viral hepatitis]. 38 66


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