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)

Although essential mixed cryoglobulinaemia (EMC) is recognized to be frequently associated with chronic liver disease, aetiology and pathogenesis of liver damage remain unsolved questions. The purpose of this study was to assess the possible causative role of hepatitis C virus (HCV) in the liver impairment occurring in patients with EMC. Twenty-six consecutive EMC patients were evaluated. All patients underwent percutaneous liver biopsy. Anti-HCV antibodies were assayed by ELISA and supported by a recombinant immunoblotting assay (4-RIBA). The prevalence of anti-HCV antibodies in patients with and without chronic active liver disease (CALD) was compared. Anti-HCV antibodies were detected in 13 patients (50%) by ELISA and confirmed in 11 of them (42.3%) by 4-RIBA, the remaining two patients being indeterminate in the supportive assay. CALD correlated significantly with anti-HCV antibodies: indeed, 7/11 (63.6%) anti-HCV+ patients showed histological and clinical pictures of CALD, compared with 1/15 (6.6%) anti-HCV- patients (P less than 0.01). With the exception of the patient who was found to be HBsAg+, no liver tissue expressed hepatitis B virus-related antigens in the hepatocytes. Additional histological findings included discrete lymphoid aggregates in portal tracts, siderosis, fatty changes, hyperplasia of Kupffer cells. It can be concluded that chronic liver damage in EMC is frequently associated with anti-HCV antibodies. Although the cause of EMC remains unknown, this study has obvious implications for clarifying the etiology of associated CALD and further supports the therapeutic use of interferons in this disease.
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PMID:Antibodies to hepatitis C virus in essential mixed cryoglobulinaemia. 153 46

As part of a study of community-acquired non-A, non-B hepatitis, liver biopsy specimens of 29 anti-HCV positive and four anti-HCV negative patients were evaluated in order to characterize the histopathologic changes of chronic hepatitis C. Liver biopsies were performed 6 to 46 mo after onset of the disease and repeat biopsies were obtained in 10 anti-HCV positive patients. The histologic diagnoses were chronic persistent hepatitis (45%), chronic active hepatitis (35%), and chronic lobular hepatitis (21%). Irrespective of the tissue diagnosis, the majority of the patients showed characteristic histologic abnormalities in the liver, particularly damage of the small and medium-sized bile ducts (76%), lymphoid aggregates in portal tracts (45%), enlarged macrophages (48%), and steatosis (31%). In 59% of the patients, two or more of these histologic abnormalities were combined. Similar histologic changes have previously been observed in non-A, non-B hepatitis, but only uncommonly in hepatitis A or hepatitis B. We conclude that the histopathologic findings in chronic hepatitis C are highly characteristic, although not pathognomonic.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Histopathology of community acquired chronic hepatitis C. The Sentinel Counties Chronic Non-A, Non-B Hepatitis Study Team. 134 9

Highly purified recombinant basic fibroblast growth factor (rbFGF) and acidic FGF (aFGF) stimulated the proliferation of human-human (h-h) hybridomas to the extent of over four-fold from a low cell density such as 1 x 10(3) cells per ml in a serum-free medium in 24-well plates. The stimulatory effect of rbFGF was also observed in various lymphoid cell lines. Expecting that FGF could be an autocrine growth factor, we introduced bFGF gene into a h-h hybridoma using an expression plasmid induced by dexamethasone. The transformed cells thus obtained, HPO-75.11 bFGF-7, were able to grow well from a low inoculum density in a serum-free medium and antibody production was also increased when bFGF gene expression was induced. The transformed cells could grow at clonal density in a serum-free medium in 96-well plates, though the original cells could not. We also obtained a more practical transfectant, HPO-75.29-H74, using a high-shear stress adapted clone as the recipient and an expression plasmid having bFGF gene under the control of metallothionein-I promoter. The HPO-75.29-H74 cells were capable of growing and producing human monoclonal antibody against hepatitis B virus surface antigen from an inoculum density of 1 x 10(3) cells per ml in an agitation vessel without addition of an inducer.
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PMID:Improvement in the proliferative activity of human-human hybridomas at low cell density by transfection with bFGF gene. 136 9

The author examined liver biopsy specimens obtained from 596 patients with chronic viral hepatitis to clarify the role of lymphoid follicle formation in the portal spaces. Lymphoid follicles were observed more frequently in chronic hepatitis non-A non-B than in chronic hepatitis B and were also common in patients with anti-hepatitis C virus-positive non-A non-B hepatitis. Immunohistology revealed that these hepatic lymphoid follicles resembled the lymphoid follicles of synovial tissue in rheumatoid arthritis. In situ hepatitis B virus markers were examined in 40 patients with chronic hepatitis B showing lymphoid follicles. Among these, hepatitis B surface antigen (HBsAg) was detected in liver cells as well as in the center of the follicles in 19 patients (47.5%). By immune electron microscopy, the author confirmed the HBsAg-positive cells in the lymphoid follicles as follicular dendritic cells. These cells appeared to be a site for antigen trapping in the follicles, therefore, the intrahepatic lymphoid follicles are suggested to play a role in immune response to HBsAg in chronic hepatitis B.
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PMID:In situ characterization of mononuclear cell phenotype in intrahepatic lymphoid follicles in patients with chronic viral hepatitis. 142 57

To determine the histologic pattern of hepatitis C, 54 liver biopsy specimens from 45 patients with a clinicopathological diagnosis of hepatitis C were studied. All patients were seropositive for antibody to hepatitis C virus by second-generation testing. Both transfusion-related and sporadic cases were included. More than half the samples showed chronic hepatitis without cirrhosis, whereas 44% showed developing or fully established cirrhosis. A histological pattern of mild chronic hepatitis with portal lymphoid follicles and varying degrees of lobular activity was found in many of the patients. Lymphoid aggregates or follicles were seen in 78% of biopsy specimens, but aggregates, less prominent than in hepatitis C, were also seen in 14 of 27 samples (52%) from patients with hepatitis B. We conclude that a characteristic histological pattern exists in chronic hepatitis C, that this pattern is not always found and that prominent lymphoid follicles, though not unique to hepatitis C, provide a useful diagnostic clue.
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PMID:The pathology of hepatitis C. 155 31

Mutations in the evolutionarily conserved codons of the p53 tumor suppressor gene are common in diverse types of human cancer. The p53 mutational spectrum differs among cancers of the colon, lung, esophagus, breast, liver, brain, reticuloendothelial tissues, and hemopoietic tissues. Analysis of these mutations can provide clues to the etiology of these diverse tumors and to the function of specific regions of p53. Transitions predominate in colon, brain, and lymphoid malignancies, whereas G:C to T:A transversions are the most frequent substitutions observed in cancers of the lung and liver. Mutations at A:T base pairs are seen more frequently in esophageal carcinomas than in other solid tumors. Most transitions in colorectal carcinomas, brain tumors, leukemias, and lymphomas are at CpG dinucleotide mutational hot spots. G to T transversions in lung, breast, and esophageal carcinomas are dispersed among numerous codons. In liver tumors in persons from geographic areas in which both aflatoxin B1 and hepatitis B virus are cancer risk factors, most mutations are at one nucleotide pair of codon 249. These differences may reflect the etiological contributions of both exogenous and endogenous factors to human carcinogenesis.
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PMID:p53 mutations in human cancers. 190 40

Transgenic mice were obtained that contained a gene of human hepatitis B surface antigen (HBsAg). The integrated HBsAg DNA sequences were inherited in the normal Mendelian fashion. 6 of 25 investigated transgenic mice expressed the HBsAg. The expression was detected in the serum and within the cytoplasm of hepatocytes. Specific tissue pathology was shown in these animals, including systemic hyperplasia of lymphoid tissue and degenerative changes in the liver and kidney parenchymatous cell elements.
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PMID:[The production and characteristics of transgenic mice expressing the surface protein gene of the human hepatitis B virus]. 217 Nov 72

The ability to introduce the cloned gene into the mouse germ line has made possible to analyze the cis-acting DNA sequence which is involved in the tissue-specific and developmental regulation of the gene. In addition, this system can also be applied to analyze the patho-physiological roles of the introduced gene product within the mouse whole body. Therefore, this system is one of the best approaches to analyze the mechanism of oncogenesis. The chromosomal translocation is one of the mechanisms leading to the activation of oncogene. In the case of lymphoid cell tumors, the reciprocal translocation between chromosome No. 8 and No. 14 is frequently observed. With this translocation, c-myc gene can be activated by the enhancer of immunoglobulin heavy chain (E mu). We and others have demonstrated that the E mu-myc gene could induce lymphomas in transgenic mice. Following these observation we have currently many examples that activated oncogene can induce variety tumors, giving basic knowledge about the relationship between activated oncogene and cell-type specificity of tumor. On the other hand, molecular mechanism of oncogenesis which is caused by viruses such as hepatitis B virus (HBV) or human T cell leukemia virus (HTLV) is totally unknown. One main reason is the absence of animal model for these diseases. To overcome this problem, we have attempted and succeeded to produce a transgenic mouse model which consistently produces HBV. Using these mice, it will be possible to elucidate the molecular mechanism of development of hepatitis and hepatocellular carcinoma.
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PMID:[Transgenic mice and their use in cancer study]. 249 65

The ultrastructural alterations induced by human immunodeficiency virus (HIV) in human lymphoid cells have been evaluated. Electron microscopic examination of peripheral blood mononuclear cells (PBMC) from 14 male homosexuals with confirmed acquired immunodeficiency syndrome (AIDS) or AIDS-related complex revealed that tubuloreticular inclusions were present in 5-15% of the cell sections from each case. In 5 of 14 cases, cylindrical confronting lamellae were found in 1-2% of the cell sections. No retrovirus-like particles or surface membrane alterations were detected. Neither of these structural alterations was observed in control PBMC obtained from six HIV-seronegative, hepatitis B virus surface antigen (HBsAg)-positive carriers or in 11 healthy subjects. When primary cultures of CD4+-enriched lymphocytes were infected in vitro with HIV, tubuloreticular inclusions could be detected in 3-10% of the cell sections, but no cylindrical confronting lamellae-like structures were found. In contrast, neither of these alterations were seen in uninfected or HIV-infected H9-HT continuous cell lines. These in vivo and in vitro studies indicate that there is an association between the appearance of the tubuloreticular inclusions and cytopathic HIV infection, although no correlation between cytopathic changes and active viral replication was observed at the single cell level. Further studies will be required to establish the mechanism(s) of formation of the tubuloreticular inclusions and to determine their prognostic potential.
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PMID:In vivo and in vitro ultrastructural alterations induced by human immunodeficiency virus in human lymphoid cells. 257 Jan 80

The presence of hepatitis B virus (HBV) and human immunodeficiency virus (HIV) was investigated using hybridization in 15 lymph nodes and one Kaposi's sarcoma skin lesion obtained from HIV-positive patients. Cryostat tissue sections were hybridized with chemically modified DNA probes for HBV and HIV. HIV genome was mainly observed in the cytoplasm of cells present in 7/15 lymph nodes and in the Kaposi's sarcoma skin lesion, thus indicating the expression of HIV replication. Control samples hybridized with an HTLV I probe were negative. HBV genome was found in the cytoplasm of lymphoid mononuclear cells in 2/7 lymph nodes, obtained from HIV+ patients without serum markers of ongoing HBV infection. Lymph node positivity for HBV DNA also confirms that lymphoid cells may be a target for HBV. Since HBV infection seems to precede HIV infection in nearly all patients, it is possible that it may represent a factor facilitating the development of the HIV-related disease.
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PMID:HBV and HIV expression in lymph nodes of HIV positive LAS patients: histology and in situ hybridization. 277 Jul 52


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