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)

Four chimpanzees have been infected with three different inocula containing "non-A, non-B" hepatitis virus(es). After inoculation, serial studies established the presence of antigenemia or viremia (or both) by radioimmunoassay with high-affinity monoclonal antibodies directed toward separate and distinct determinants on hepatitis B surface antigen (HBsAg) and by molecular hybridization analysis using a cloned hepatitis B virus (HBV) DNA probe. In contrast to results observed during HBV infection, elevations in serum alanine aminotransferase values indicate that liver injury preceded antigenemia by several weeks. Thus, the time between inoculation and development of antigenemia (incubation period) varied from 64 to 190 days and, in some cases, single or multiple episodes of antigenemia or viremia occurred in the absence of elevated aminotransferase levels. In this study, two chimpanzees were high-titer positive for antibodies to HBsAg (anti-HBs) from previous infection with HBV, suggesting that the antigenic composition of HBV-related virus(es) is substantially different from that of HBV, since naturally occurring anti-HBs antibodies were not protective. Demonstration of HBV-related virus(es) by the methods used in this study of experimental hepatitis infection in chimpanzees should now permit detection, isolation, and characterization of these previously elusive agents.
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PMID:Detection and transmission in chimpanzees of hepatitis B virus-related agents formerly designated "non-A, non-B" hepatitis. 681 47

A radioimmunoassay is described for detection of IgM antibody to the hepatitis B core antigen. The assay is based on the selective absorption of IgM immunoglobulins from test serum by anti-IgM fixed on a solid phase, followed by incubation with HBcAg and radiolabeled anti-HBc of IgG type. IgM anti-HBc was found in high titers in all the patients with acute hepatitis B; in two of four patients whose acute hepatitis progressed to chronicity, IgM anti- HBc disappeared in 4-6 months despite continuing HB viremia. IgM anti-HBc was also found in low titers in 19% of the patients with chronic HBV infection. No relation was noted between the presence of IgM anti-HBc and clinical or serological categories of chronic carriers of the HBsAg. The antibody was not found in carriers with hepatitis caused by superinfection with the hepatitis A virus or the HBV-associated delta agent. IgM anti-HBc is a marker of a recent HBV infection. Its absence in HBsAg-positive individuals with acute hepatitis should rise suspicion that the patients are carriers of the HBsAg experiencing disease caused by factors other than the HBV.
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PMID:Radioimmunoassay detection of IgM antibodies to the hepatitis B core antigen in HBsAg liver disease. 698 22

Variations in the serum levels of hepatitis C virus (HCV) RNA. IgM antibody against the HCV 'core' structural protein (c22) and alanine amino-transferase (ALT) were measured in 23 patients with chronic hepatitis C who underwent therapy with interferon-alpha 2a (IFN alpha 2a). Low pretreatment levels of viraemia and undetectable IgM anti-core were significantly associated with a long-term response to treatment. In patients with hepatitis relapses after the end of treatment, HCV RNA levels increased before or at the same time as ALT in 29 out of 34 cases (85%). ALT flares occurred before or simultaneously with IgM anti-core elevations in 18 out of 20 cases (90%). Therefore, post-treatment hepatitis C exacerbations show the same sequence of events seen as in hepatitis B exacerbations (increases of viraemia followed by those of ALT and IgM anti-'core'). These findings underscore the diagnostic and prognostic usefulness of monitoring anti-HCV-positive patients with quantitative assays for HCV markers.
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PMID:The fluctuations of hepatitis C virus RNA and IgM anti-HCV (core) serum levels correlate with those of alanine aminotransferases during the hepatitis relapses of patients treated with interferon. 748 43

Hepatitis C virus (HCV) infection is the leading cause of post-transplant non-A, non-B hepatitis. Although many end-stage renal disease patients present for transplantation already infected with HCV, some recipients acquire the infection by transmission from the donor organ. We have detected serological evidence for HCV infection in 6.8% of our organ donors using second-generation anti-HCV assays. Approximately one-third of the patients who received an organ from a HCV carrier donor developed chronic transaminasemia and 8 of 14 (56%) patients converted from HCV RNA negative to positive in the posttransplant period. Demonstration of the course of viremia and transaminasemia is presented for 2 patients in whom transmission of HCV occurred. Using pulsatile machine perfusion, we were able to demonstrate that a standard perfusion of 20 h reduced the viral load in the kidney by 75%, additional flushes and a subsequent perfusion reduced the total viral titer by more than 99%. Thus, although transmission of HCV does occur with solid-organ transplantation, differences in the incidence of transmission between centers may be related to techniques of organ preservation.
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PMID:Transmission of hepatitis C virus by kidney transplantation: impact of perfusion techniques and course of viremia post transplant. 749 83

In chronic hepatitis B virus (HBV) infection seroconversion from hepatitis B e antigen (HBeAg) to hepatitis B e antibody (HBeAb) may be followed either by remission of the disease with low-level viraemia, or by continuing inflammation with high-level viraemia. In both situations the virus may acquire a mutation in the precore sequence which prevents it from encoding HBeAg. We now show that the number of amino acid substitutions in the HBV core is low in viral sequences from patients with HBeAg positive chronic liver disease and HBeAg negative HBeAb positive patients in remission, but the frequency of substitutions is high in HBeAg, negative HBeAb positive patients with active liver disease. Furthermore we show that these substitutions cluster in the promiscuous CD4+ T-helper-cell epitope and in HBV core/e antibody binding determinants, but are not found in regions recognized by major histocompatability complex (MHC) restricted cytotoxic T lymphocytes. Sequential viral sequences from patients before and after HBeAg/HbeAb seroconversion shows that core mutations arise either at the same time or after the precore stop mutation which prevents the virus from encoding HBeAg. These results are consistent with the hypothesis that after clearance of HBeAg, mutations in regions of the virus recognized by CD4+ helper T cells and B cells allow persistence of the HBe negative virus in HBeAb positive patients with viraemia and active hepatitis.
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PMID:Hepatitis B e antigen negative chronic active hepatitis: hepatitis B virus core mutations occur predominantly in known antigenic determinants. 749 1

Five Swedish patients with chronic hepatitis C were prospectively followed until hepatocellular carcinoma (HCC) developed. Hepatitis C virus (HCV) antibodies were analysed by a second generation anti-HCV ELISA and a recombinant immunoblot assay (RIBA-2) and viraemia by detection of serum HCV RNA by polymerase chain reaction. Four patients had post transfusion hepatitis and in one patient the source of infection was unknown. HCC developed after 8 to 23 years of mostly asymptomatic disease and all patients died. Four of them were repeatedly biopsied during follow-up and all had chronic active hepatitis. When HCC was diagnosed, cirrhosis was present in all 5. In 4 patients with available sera, anti-HCV was positive and confirmed with RIBA-2, whereof 2 were reactive only to the c-22 and c-33c epitopes. HCV-RNA was present in all sera when HCC was diagnosed. Thus, after prolonged disease duration these patients were still viraemic.
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PMID:Hepatitis C virus infection with progression to hepatocellular carcinoma: a report of five prospectively followed patients in Sweden. 750 21

In November 1989, Japanese Red Cross Blood Centres started screening for hepatitis C virus (HCV) with enzyme-linked immunosorbent assay (Elisa) for the C100-3 viral peptide as the first such nationwide programme in the world. Thereafter post-transfusion non-A non-B hepatitis (PTNANBH) was reduced by 61-80%, but this was not as complete a success as our programme to prevent post-transfusion hepatitis B by screening for high titer hepatitis B core antibody, which we began in the same period. In order to acquire more effective control of PTNANBH, the HCV core-related antigen (GOR, N14) and second-generation Elisa (Ortho2, Abbott2) and second-generation antigen agglutination (PA, PHA) tests have been employed. Among 16,500 donors in 11 blood centers, 365 were serologically positive by at least one of these tests. Among these, HCV RNA was detected in 138 units and the remaining 227 were HCV RNA negatives. The effectiveness of these serological tests to detect HCV RNA-positive status were analyzed. Passive haemagglutination and particle agglutination (PHA and PA) tests were highly effective to predict HCV viraemia among blood donors. Also, these tests can easily determine antibody titre. By either PHA or PA, all units with > or = 2(12) agglutination titre (120 and 122 units) were HCV RNA positive and all agglutination-positive units with serum alanine aminotransferase level higher than 35 Karmen units were HCV RNA positive.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Predictive value of screening tests for persistent hepatitis C virus infection evidenced by viraemia. Japanese experience. 750 73

One hundred renal transplant recipients were studied for antibodies to hepatitis C virus (HCV), and to HCV RNA in serum by reverse transcription+nested polymerase chain reaction (RT-PCR). Presence of antibody to HCV confirmed by recombinant immunoblot assay II was considered evidence of HCV infection, and detection of HCV RNA by RT-PCR was considered evidence for active viremia. On pretransplant sera, 18 patients were RT-PCR positive and an additional 3 had antibody evidence of HCV infection. At 1-year follow-up, all of these patients were RT-PCR positive and an additional 7 patients became RT-PCR positive. Clinical diagnosis of non-A, non-B hepatitis underestimated the prevalence of HCV infection (5/28 cases, 18%). Serum alanine aminotransferase (ALT) elevations were neither sensitive nor specific. An isolated pretransplant ALT elevation predicted a 52% chance of being RT-PCR positive for HCV. An ALT elevation greater than 2 months after transplant predicted a 45% chance of HCV positivity; however, 18% of patients who never had any ALT abnormality were also HCV positive. Sixty-eight patients had an early postoperative rise in ALT, but there was no correlation with HCV status. After an average follow-up of over 4 years, 3/28 HCV-positive patients developed cirrhosis. HCV infection in the renal transplant population is common and underdiagnosed by clinical and biochemical parameters. HCV appears not to cause aggressive liver disease in the early posttransplant period, but longer follow-up is needed to define the natural history of HCV in the renal transplant population.
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PMID:Non-A, non-B hepatitis and elevated serum aminotransferases in renal transplant patients. Correlation with hepatitis C infection. 750 51

Hepatitis C virus (HCV) infection was studied in 60 liver transplant recipients. Antibodies to HCV were tested by both a second-generation ELISA test and a four-recombinant immunoblot assay (4-RIBA) just before the transplant and every three months thereafter. HCV RNA detection was performed by polymerase chain reaction (PCR) at least three times after the transplant in all the patients. Thirty-nine patients tested negative by ELISA before LT (group A), 14 patients tested positive by both serological tests (group B), and seven tested positive only by ELISA (group C). Posttransplant hepatitis was diagnosed in 11/14 in group B in comparison with 3/39 in group A (P < 0.001) and 1/7 in group C (P < 0.05). HCV RNA was detected in the sera of 14/14 patients in group B but in only 1/7 in group C and 6/39 in group A. Only 2/15 patients developed posttransplant hepatitis in the absence of HCV RNA detection. These data suggest that HCV is the major cause of hepatitis after LT. Patients HCV seropositive by RIBA test before the transplant formed a group of high-risk patients for developing viremia and hepatitis afterwards.
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PMID:Clinical significance of hepatitis C virus (HCV) infection in liver transplant recipients. Role of serology and HCV RNA detection. 751 32

Until 1988 the putative agent of non-A/non-B (NANB) hepatitis had not been found. Research workers of the Chiron Corporation (California, USA) then identified, by "blind expression cloning", polypeptides which specifically bound antibodies present in sera of NANB-patients. A fusion polypeptide (C-100) was expressed in yeast. With the C-100 antigen prototype RIA and ELISA antibody tests were developed. Subsequently more polypeptides (C-200, C33c, C22) of the HCV-genome were added to the test system, resulting in second generation anti-HCV tests with increased sensitivity. For confirmation of HCV ELISA reactive samples, recombinant immunoblot (RIBA-2, Ortho; Innolia, Innogenetics) and dot immunoblot assays (Matrix, Abbott) were developed. Detection of HCV antigens has been hampered by the low virus titres in serum and the absence of free circulating viral antigen(s). However, with cDNA-PCR, applying primers of the highly (> 93% nucleotide homology) conserved 5' untranslated (5'UTR) region of the HCV genome, HCV-RNA in serum as well as in liver tissue can be detected. cDNA-PCR, although not yet commercially available, is useful to confirm HCV-viremia in patients. When chronic hepatitic C patients are treated with anti-viral drugs, the disappearance of HCV-RNA, as detected by PCR, is a measure of therapy response.
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PMID:Testing for HCV markers. 751 61


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