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)

Tubuloreticular inclusions (TRI) developed within the endoplasmic reticulum of peripheral blood mononuclear cells (PBMC) sampled from eight patients with chronic type B hepatitis during cycles of therapy with DNA-recombinant human alpha-interferon (rIFN alpha A). Each cycle of therapy consisted of a series of six intramuscular injections (triweekly) of a fixed dose of rIFN alpha A (from 18 to 68 X 10(6) IU/dose). In PBMC examined by transmission electron microscopy, TRI were absent prior to therapy and developed during therapy in all cases. Peak serum levels of alpha-interferon (320 to 960 IU/ml) were achieved within 12 hours. At 24 hours. TRI were detected in 0.5 to 6.5% of PBMC sections, and they persisted in 1.4 to 6.8% of sections examined at 48 hours. After five sequential interferon doses, TRI were observed in 1.6 to 9.8% of PBMC sections. TRI could no longer be detected at 5 to 16 days after cessation of rIFN alpha A, but they reappeared during subsequent cycles of therapy. Subpopulations of the PBMC with TRI were differentiated by immunoelectron microscopy utilizing a battery of anti-Leu monoclonal antibodies: surface markers of T cells, helper/inducer or cytotoxic/suppressor T cell subsets, natural killer cells, or B-cells were identified by direct or indirect procedures utilizing avidin and biotinylated peroxidase. In cases analyzed with multiple monoclonal antisera, TRI were expressed in all of the major PBMC subpopulations. Monocytes with TRI were demonstrated by the endogenous peroxidase reaction. TRI were not found in circulating polymorphonuclear granulocytes. Lymphocytes isolated from healthy donors and exposed to rIFN alpha A (100 IU/ml), for 48 to 72 hours in vitro, developed TRI in proportions of PBMC sections (2.3 to 8.4%) comparable to those observed in the interferon-treated patients. Stimulation of lymphocytes with concanavalin A, for 72 hours before rIFN alpha A exposure, enhanced formation of TRI which could then be found in T blasts. Stimulation of donor lymphocytes with Sendai virus, a potent inducer of alpha-interferon, also resulted in formation of TRI by 48 hours. This suggested that lymphocytotrophic virus infections could exercise a primary role in the natural pathogenesis of TRI.
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PMID:Tubuloreticular inclusions in peripheral blood mononuclear cells related to systemic therapy with alpha-interferon. 389 55

On the occasion of an outbreak of non-A, non-B hepatitis in a plasmapheresis centre (81 cases, incubation period: 3--6 weeks) a pool of 12 plasma samples was obtained in the early phase of increasing transaminases. Two chimpanzees were inoculated, each receiving 12 ml of the pooled plasma. After an incubation period of 10--12 weeks a mild non-A, non-B hepatitis developed. Serum transaminases were slightly elevated. Needle biopsies, taken fortnightly, showed a slight activation of Kupffer cells (6--8 weeks), single cell necroses, and infiltration of the portal tracts (10--13 weeks). Electron microscopically four types of cytoplasmic change, were found in hepatocytes and assumed to be specific for the infection, Type I: Sponge-like inclusion (6 weeks after inoculation) composed of a dense matrix and irregularly arranged membranes. Type II: Attaching curved membranes (8 weeks), developing by close apposition of two cisternae of smooth endoplasmic reticulum. Type III: Cylindrical complexes (10 weeks), already described in literature. Type IV: Microtubular aggregates, usually neighbouring type III structures. The findings suggest 1) that the agent of the present infection is, at least in part, identical with that of the long incubation type of experimental non-A, non-B hepatitis, and 2) that ultrastructural alterations may precede manifest hepatitis.
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PMID:Experimental non-A, non-B hepatitis: four types of cytoplasmic alteration in hepatocytes of infected chimpanzees. 611 Feb 71

The intracellular sites of biosynthesis of the structural proteins of murine hepatitis virus A59 have been analyzed using cell fractionation techniques. The nucleocapsid protein N is synthesized on free polysomes, whereas the envelope glycoproteins E1 and E2 are translated on the rough endoplasmic reticulum (RER). Glycoprotein E2 present in the RER contains N-glycosidically linked oligosaccharides of the mannose-rich type, supporting the concept that glycosylation of this protein is initiated at the co-translational level. In contrast, O-glycosylation of E1 occurs after transfer of the protein to smooth intracellular membranes. Monensin does not interfere with virus budding from the membranes of the endoplasmic reticulum, but it inhibits virus release and fusion of infected cells. The oligosaccharide side chains of E2 obtained under these conditions are resistant to endoglycosidase H and lack fucose suggesting that transport of this glycoprotein is inhibited between the trans Golgi cisternae and the cell surface. Glycoprotein E1 synthesized in the presence of monensin is completely carbohydrate-free. This observation suggests that the intracellular transport of this glycoprotein is also blocked by monensin.
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PMID:Post-translational glycosylation of coronavirus glycoprotein E1: inhibition by monensin. 632 72

Sera from 5154 subjects comprising patients with liver diseases (n = 1311), immunological and connective tissue disorders (n = 1098) and other diseases (n = 2421), and healthy people (n = 324), were investigated by immunofluorescence for IgG antibodies (titre greater than or equal to 1:20) against mitochondria (AMA), endoplasmic reticulum (AER), nonorganspecific ribosomes (ARA-1), and liver typical ribosomes (ARA-2). AMA were classified in 10 subtypes. AMA (n = 163 = total 3.2%) were found predominantly in liver diseases (n = 101 = 7.7%) and in autoimmunopathies (n = 34 = 3.1%). AER (n = 59 = total 1.1%) were detected mainly in liver diseases (n = 40 = 3%), ARA-1 (n = 14 = total 3%) in autoimmunopathies (n = 7 = 0.64%), and ARA-2 (n = 7 = total 0.14%) exclusively in liver diseases (n = 7 = 0.5%) (acute and chronic relapsing hepatitis with viral markers). The diagnostic value of antibodies depends among other things on the titre and the subtype. AMA of type 2 and 4 with a titre higher than 1:1280 are a valuable marker of primary biliary cirrhosis or a related disease, even in the absence of other diagnostic signs. AER with a titre higher than 1:320 suggest a special form of autoimmune chronic hepatitis with rapid progress to liver cirrhosis. The diagnostic value of other antimitochondrial antibodies (especially those of type 5 to 10) and of antiribosomal antibodies is not exactly known.
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PMID:[Diagnostic significance of antibodies against cell organelles (mitochondria, endoplasmic reticulum and ribosomes)]. 633 82

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

Two separate and distinct episodes of non-A, non-B hepatitis were induced in each of two chimpanzees by two inocula: one containing a chloroform-resistant agent and the other containing a chloroform-sensitive agent. Both agents were recovered from liver tissue and plasma obtained from a single chimpanzee during the acute and chronic phases of infection with a factor VIII concentrate, respectively. The chloroform-resistant agent did not cause unique changes in hepatocytes; in contrast, the chloroform-sensitive agent did induce the formation of cytoplasmic tubules, convoluted endoplasmic reticulum, and dense reticular inclusion bodies. The latter changes are similar in character to those induced in infected cells by some enveloped mammalian RNA viruses.
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PMID:Posttransfusion non-A, non-B hepatitis: physicochemical properties of two distinct agents. 641 32

Heroin abusers are frequently found to have abnormal liver function tests and hepatic histology. Hepatitis viruses A, B, and NANB, other drugs or drug contaminants and excessive alcohol consumption are factors thought to contribute. One hundred and sixteen heroin abusers attending a London treatment centre were studied. Sixty two (53%) had a raised aspartate transaminase. This was not explained by current infection with hepatitis A and B, cytomegalo or Epstein-Barr viruses, excessive alcohol consumption (greater than 80 g/day) or concomitant drug taking. Abnormal liver function tests were as frequent in those with markers of current or past HBV infection as those without and there was evidence that both HBV infection and the cause of the abnormal liver function tests were acquired in the first few years of intravenous drug abuse. Liver biopsies from eight patients showed chronic hepatitis with a mild lobular and portal inflammatory infiltrate, fatty change and prominent sinusoidal cells. Electron microscopy showed cytoplasmic trilaminar tubular structures and dense fused membranes in dilated endoplasmic reticulum. These clinical, biochemical, serological, and histological features would suggest a major role for NANB virus infection in the aetiology of hepatitis in heroin abusers.
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PMID:Clinical, biochemical, serological, histological and ultrastructural features of liver disease in drug abusers. 642 58

Ultrastructural findings in the liver of a 52-year-old man with acute non-A, non-B (NANB) post-transfusion hepatitis are described. Apart from non-specific alterations also known to occur in hepatocytes in hepatitis A and B--such as proliferation of membranes of smooth endoplasmic reticulum, formation of membrane-bound cytoplasmic vacuoles containing electron-dense material, and accumulation of distorted peroxisomes--unique cytoplasmic changes were observed that have not previously been described in man. A few hepatocytes contained in their cytoplasm tightly packed, bent, parallel structures and small clusters of virus-sized particles. No virus-like material was found in the nucleus of liver cells or in Kupffer and endothelial cells. Closely similar structures have been reported earlier in the acute-phase hepatocytic cytoplasm of chimpanzees with NANB hepatitis. These alterations may represent an ultrastructural hallmark of acute human NANB hepatitis.
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PMID:Ultrastructural changes in human hepatocytes in acute non-A, non-B hepatitis. 642 27

In experimental toxic hepatitis induced by injection of CCl4 into rats, the rat blood and urine content of acetylated sulfamonomethoxine diminishes, the acetylation of sulfamonomethoxine and norsulfazole in an isolated stomach of the rat reduces, and acetylation of sulfamonomethoxine is inhibited by rat liver and small intestine homogenates. This confirms that different types of pathology (infectious and non-infectious) provoke the same line of changes, namely the reduction of acetylation of sulfanilamide substances in the body. CCl1 decreases sulfamonomethoxine acetylation by a mixture of the mitochondria and microsomes of the rat liver, i. e. eliminates the synergistic effect characteristic for intact rats. The reduction of acetylation recorded at different levels of the organization of the living systems--bodily, organ and subcellular ones--is accounted for by the lowering of the acetylcoenzyme A content in the tissues. One of the reasons for reduction of acetylation during the CCl4-induced liver injury lies in the impairment in the liver cells of the interaction between the mitochondria and endoplasmic reticulum.
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PMID:[Acetylation of sulfanilamide substances in toxic lesions of the liver]. 650 37

Seven patients with diagnosis of biliary atresia (BA) and two patients with neonatal hepatitis were studied by electron microscopy. In all patients the diagnosis was done by clinical examinations, laboratory assays, histological studies by punch or surgical biopsies and or surgical examinations combined with intraoperatory cholangiography. The ultrastructural alterations found in both groups of patients were essentially similar to those described in other forms of cholestasis. In patients suffering from biliary atresia the main features found at hepatocytic livel were: Finely granular deposits of electron dense substance sometimes conforming lamellar structures; 2) Some increase and vesiculation of smooth endoplasmic reticulum membranes; 3) Reductions in number and length of sinusoidal microvilli; in some areas was also detected basal membrane and an increase in the amount of collagen fibers in the space of Disse; 4) Marked bile canaliculi dilatations with reduction of microvilli and thickening of the pericanalicular surrounding area, some canaliculi were constitued by several hepatocytes. Ductules were found in only 3 cases with the following alterations: 1) Intracytoplasmic electron dense deposits of granular material without limiting membranes; 2) A marked increase in the number of microfilaments mainly located in the apical portion of the cell or in the vicinity of the nuclei; 3) Inflammatory cells in the duct epithelium or in direct contact with the hepatocytes. The ultrastructural findings in the two cases of neonatal hepatitis (NH) resembled those described in the biliary atresia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Liver ultrastructure in congenital atresia of the extrahepatic bile ducts]. 653 1


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