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)

A new rapid serologic enzyme immunoassay for antibodies to hepatitis C virus (HCV) is described. The assay combines synthetic peptide and recombinant antigens representing putative structural and non structural HCV gene products with paramagnetic microparticle assay (MP assay) technology. Assay readout is based upon an enzymatically generated fluorescent product which is quantified with a novel semi-automated washer/reader instrument system. Assay sensitivity and specificity was determined to be greater than the first generation HCV C-100 EIA using a non-A, non-B hepatitis disease panel, an HCV performance panel, an HCV seroconversion panel, dilutions of HCV reactive sera, and random volunteer blood donor specimens.
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PMID:A novel semi-automated paramagnetic microparticle based enzyme immunoassay for hepatitis C virus: its application to serologic testing. 132 58

The clinical features of 'cryptogenic' chronic liver disease and the prevalence of antibody to hepatitis C virus (HCV) in serum have been investigated in 33 Italian children (mean age 5 years). The diagnosis was based on the persistence of increased alanineaminotransferase values for longer than 6 months after the exclusion of biliary diseases, of extra-hepatic causes of hypertransaminasemia, of infection with known hepatotropic viruses and of autoimmune or metabolic disorders. Five patients had been transfused early in life, three had undergone surgery and one girl's mother had had acute non-A, non-B hepatitis during pregnancy. The remaining patients had no history of overt parenteral exposure. At presentation only 11 patients were symptomatic, the others had been referred after a check-up for intercurrent diseases. Liver histology performed in 21 cases showed persistent or mild active hepatitis in 18 cases and severe hepatitis or cirrhosis in three cases. Anti-HCV antibodies were found in 48% of the cases, including 88% with obvious exposure and 33% of the remaining cases. During a mean follow-up period of 5 years (range 1-14 years) only 11% of the cases achieved sustained biochemical remission, although none developed signs of liver failure. There was no significant difference in the clinical features and outcome of the disease between anti-HCV-positive and -negative patients. The results of this study suggest that HCV is implicated in most cases of 'cryptogenic' chronic liver disease observed in Italian children with a history of parenteral exposure and in at least one-third of the cases without overt exposure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cryptogenic chronic liver disease and hepatitis C virus infection in children. 132 75

The molecular properties of the genomes of both hepatitis C virus (HCV) and hepatitis E virus (HEV), the major etiologic agents of non-A, non-B hepatitis, are briefly described. The organization of the genome of each of these viruses is discussed and compared to those of other related or distantly related viruses that contain single-stranded, positive-sense RNA genomes. In the case of HEV, the reactivity of expressed proteins and genetic divergence of geographically distinct isolates are also described within the context of sequence variation, type-common epitopes and type-specific epitopes.
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PMID:Recent developments in the molecular cloning and characterization of hepatitis C and E viruses. 132 75

Human hepatitis B virus (HBV) carriers run an increased risk of hepatocellular carcinoma (HCC), where the expression of HBV genes play the most important role in the initial stage of hepatocarcinogenesis. As the integration of HBV DNA into the cellular DNA of HCC as well as chronic hepatitis was demonstrated very frequently, the virus-cell fusion gene was considered to be most essential for hepatocarcinogenesis. Among the virus-cell fusion genes, the X gene is known to function as a transactivator for viral and cellular genes at the time of chronic infection. One mechanism for hepatocarcinogenesis that appears particularly reasonable is transactivation of cellular oncogenes by the X-cell fusion protein. In 1990, we found a part of the amino acid sequences in the X protein to be highly homologous to functionally essential sequences in the Kunitz domain, characteristic of Kunitz-type serine protease inhibitors. It has been recently demonstrated that X protein expressed in E. coli or from the in vitro translation system binds to a specific serine protease from the liver cells. These results indicate that transactivation function of X protein may be exerted by acting as a protease inhibitor analogue to control the proteolytic pathway of cellular transcription factor(s). On the other hand, viral hepatitis resulting from viruses other than hepatitis A virus and HBV has been referred to as non-A, non-B hepatitis. In 1989, the viral genome was molecularly cloned as a positive-strand RNA having about 10 kb in size and named as hepatitis C virus (HCV). Details of genetic structure and mechanism of expression are currently under investigation at molecular level.
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PMID:[Gene expression of hepatitis viruses in the liver and hepatocarcinogenesis]. 132 91

All heart transplant patients in our clinic received intravenous immunoglobulins as a prophylaxis against cytomegalovirus infections or reactivations. Serum was sampled from 160 heart transplant patients within 4 months after surgery. In 98 samples (61%) hepatitis C virus (HCV)-specific antibodies could be detected by a "second generation" enzyme immunoassay. Of these HCV antibody-positive patients 89 were tested for a second time. At this time, 5-11 months later, in 66 patients (74%) the HCV antibody had disappeared. In the 23 still positively reacting patients, immunoglobulins were given in the last 6 months before serum sampling. Nine commercial immunoglobulin preparations were tested for HCV-specific antibodies and the presence of HCV RNA. Seven preparations were anti-HCV positive with titres in the range of 64-256, whereas reverse transcription and polymerase chain reaction did not detect HCV RNA in any immunoglobulin preparation. Passive antibody transfer rather than a HCV infection is the cause of HCV antibody detection in our patients. The presence of HCV antibodies in high concentrations in commercial immunoglobulin preparations may only be explained by an extremely high proportion of anti-HCV-positive single donations in the plasma pools used for immunoglobulin production. The passive HCV antibody transmission prevents anti-HCV serological monitoring of patients treated with these preparations. Additionally, there are reports on the transmission of hepatitis non-A, non-B via immunoglobulin preparations. Therefore, we recommend an anti-HCV screening of plasma donors.
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PMID:Immunoglobulin preparations from hepatitis C antibody-positive plasma donors: influence on diagnosis and risk of infection in heart transplant recipients. 132 28

We evaluated the prevalence of hepatitis C virus (HCV) RNA and antibody (anti-HCVcore) to the putative HCV core protein in Japanese patients with chronic liver disease. Sera were screened by solid-phase enzyme immunoassay with a recombinant HCV core protein and by the reverse transcription-polymerase chain reaction (RT-PCR) test which directly detects the HCV genome. Anti-HCV core was detected with high titers in 95% (69/73) of chronic non-A, non-B hepatitis, and 94% (65/69) of anti-HCVcore-positive patients had the genome. Anti-HCVcore was also found with lower titers in 24% (10/41) of chronic hepatitis B virus carriers, and three of them had the genome. Only one (3%) of the 35 patients negative for anti-HCVcore tested positive to RT-PCR. These findings indicate the overwhelming prevalence of HCV infection in Japanese patients with chronic non-A, non-B hepatitis and a close relationship between the presence of anti-HCVcore and chronic hepatitis C in this population.
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PMID:HCV RNA and antibody to HCV core protein in Japanese patients with chronic liver disease. 132 84

The antibody to hepatitis C virus (anti-HCV) was measured by an immunoassay in 507 serum samples from 94 patients with acute and chronic post-transfusion non-A, non-B hepatitis (NANB) and in 436 healthy blood donors. Anti-HCV was found in 70.8 of patients with acute hepatitis, in 78.2 with chronic hepatitis, and in 1.4 of healthy blood donors. In acute hepatitis, anti-HCV appeared in the serum from 4 to 34 weeks after transfusion and from 1 to 30 weeks after the onset of the overt disease. Three patients with resolving hepatitis (21%) and 2 who developed chronic hepatitis (10%) lost anti-HCV during a mean follow-up period of 28 months. Among the 36 patients with chronic hepatitis, 2 (6%) lost anti-HCV after 12 months and 8 years respectively. These data indicate that in recent years HCV has been the major etiologic agent of acute and chronic transfusion-associated hepatitis (TAH) in our geographical area. The late appearance of anti-HCV from the onset of clinical and biochemical signs of acute hepatitis in more than 70% of patients limits the diagnostic utility of this assay for an earlier serological diagnosis of acute NANB hepatitis. Additional studies are required to determine the diagnostic significance of this antibody in chronic NANB hepatitis.
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PMID:Development of antibody to hepatitis C virus (HCV) in acute and chronic non-A, non-B post-transfusion hepatitis. 132 65

Twelve children with chronic non-A, non-B hepatitis were entered in a pilot trial of recombinant interferon-alpha. Although all the children had hepatitis C virus RNA in serum, only five had antibodies against this virus. Children received 3 MU/m2 body surface area interferon-alpha 3 times/wk for 6 mo; they were followed for 24 mo, including the therapy period. One child was dropped from the study, so the results are from the 11 children who completed the study. At the end of the therapy period, 36% of the children had normal ALT levels; this percentage increased to 90% at mo 15 of follow-up. Thereafter, relapse occurred in five children; thus ALT normalization was observed in 5 of 11 children at the 24th month. Moreover, two different ALT patterns were found: HCV antibody-negative children had significant peaks of ALT levels with respect to the basal samples (p less than 0.05) until the third month of the therapy; these levels later decreased. In contrast, HCV antibody-positive children had slight fluctuations of ALT until normal levels were reached. At the end of treatment, three children had HCV RNA; one demonstrated a rebound in ALT levels. Finally, histological activity had decreased significantly in the second liver biopsy specimen in all children. In summary, interferon treatment in children with chronic hepatitis C may be helpful, although these results should be confirmed in controlled trials.
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PMID:Treatment of children with chronic hepatitis C with recombinant interferon-alpha: a pilot study. 132 9

The prevalence of hepatitis C virus (HCV) infection was estimated in a 14-month study using anti-C100-3 antibody assay in 31 HBsAg negative patients on maintenance hemodialysis (MHD) for > or = 3 months. One and three patients respectively had ALT elevation and anti-HCV positivity at entry. During MHD (mean period of follow up 9.9 mo), 11 (35.5%) patients had, on fortnightly estimation, ALT elevation which lasted for < or = 6 months in seven patients and for > 6 months in four. Fourteen (45.2%) patients had anti-HCV (including the three positive at entry). There was no significant difference in frequency of anti-HCV positivity in patients with normal and elevated ALT (57.1% and 42.9% respectively). The number of blood transfusions and duration of MHD were similar in anti-HCV positive and anti-HCV negative patients. We conclude that our MHD patients have a high frequency of hepatitis and anti-HCV positivity, and these may not be related to blood transfusions.
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PMID:Prevalence of antibodies to hepatitis C virus in HBsAg negative hemodialysis patients. 132 45

Complementary DNA clones corresponding to one of the putative structural regions of the hepatitis C virus (HCV) genome were obtained from sera of non-A non-B hepatitis patients. The putative envelope gene was expressed by using a recombinant vaccinia virus carrying this region of the HCV genome. In cells infected with the recombinant vaccinia virus, a glycosylated protein with an M(r) of about 35K (gp35) was specifically detected by convalescent sera from hepatitis C patients. The sera from rabbits immunized with this recombinant vaccinia virus reacted to the gp35 produced in insect cells and also to gp35 which was translated in vitro in the glycosylated and processed form. The gp35 was used to detect antibodies in sera of only 7 to 23% of HCV patients at various stages of HCV disease. These results suggest that the gp35 of HCV may not have high antigenicity in humans.
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PMID:Expression and characterization of glycoprotein gp35 of hepatitis C virus using recombinant vaccinia virus. 132 87


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