Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.6.1.2 (alanine aminotransferase)
26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An enzyme-linked immunosorbent assay (ELISA) was developed for serological diagnosis of hepatitis C virus (HCV) infection, using HCV core protein (p22) synthesized by a recombinant baculovirus. Among 58 clinically well-defined chronic non-A, non-B hepatitis (NANBH) patients, 49 (84.5%) were positive for p22 antibody (anti-p22), whereas 42 (72.4%) were positive for C100-3 antibody (anti-C100-3), as measured by the present assay using the HCV nonstructural protein as antigen. Thirty-nine patients (67.2%) had both antibodies. No significant level of anti-p22 was detected in sera of chronic hepatitis B patients or normal blood donors. In typical post-transfusion NANBH patients, anti-p22 could be detected at, or even before, the first alanine aminotransferase peak. Anti-p22 was also detected in blood donors who were previously shown to be involved in transmitting HCV but in whose serum anti-C100-3 was not detectable. The ELISA detecting antibody to the HCV core protein expressed and properly processed in animal cells will be useful for mass screening of donor blood as well as for early diagnosis of hepatitis C.
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PMID:Serodiagnosis of hepatitis C virus (HCV) infection with an HCV core protein molecularly expressed by a recombinant baculovirus. 190 12

To determine the prevalence and clinical significance of IgM and IgA antibody to hepatitis C virus (HCV) core antigen in chronic HCV infection, sera from 47 patients were tested for immunoglobulin class M (IgM) and immunoglobulin A (IgA) antibody to HCV core antigen by solid-phase enzyme-linked immunoassay using a recombinant core protein (aa1-150). Results were correlated with the clinical, biochemical and histological parameters, serum HCV RNA levels (determined by branched DNA signal amplification assay), and subsequent clinical response to interferon-alpha therapy. IgM anti-HCV core was detected in 11 patients (23.4 percent). There was no correlation between the presence of IgM anti-HCV core and the clinical features (sex, age, mode of acquisition), biochemical parameters (serum ALT, AST, alkaline phosphatase, and albumin level), autoimmune markers [serum globulin levels, anti-nuclear antibody (+ at < 1:80 in 7/47 patients)], serum HCV RNA levels, subsequent response to interferon-alpha therapy, and the histological features. Immunoglobulin A anti-HCV core was not detected in any of the patients. The presence of IgM ant-HCV core in a proportion of patients with chronic HCV infection indicates that the presence of serum IgM anti-HCV core may not be unique to acute HCV infection.
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PMID:Immunoglobulin M and A antibodies to hepatitis C core antigen in chronic hepatitis C virus infection. 752 59

Hepatitis C virus (HCV) infection can be diagnosed by antibody assay systems using recombinant antigens since the HCV genome has been identified. It is still impossible to detect viral antigens associated with HCV. Therefore, the polymerase chain reaction (PCR) has been widely used in practical laboratory examinations. Because HCV is an RNA virus and the reverse transcription process is required prior to the PCR reaction, the process of HCV RNA detection has a risk of contamination and the detection rate may differ with the PCR condition. There are several genome diagnostic methods for HCV infection; that is, genome detection by nested PCR, HCV subtyping using mixed primer, quantitation of HCV genome using competitive PCR, Quant-Amp and branched DNA probe. To clarify what factors are responsible, the efficacy of interferon therapy against chronic hepatitis C was examined. The normalization rate of serum ALT level and clearance rate of HCV RNA in serum at six months after the end of the treatment were correlated to the titer of HCV RNA genome and the HCV subtype. The patients with HCV RNA titers of less than 10(4) copies/50 microliters and with subtype group III showed a high response to interferon administration. On the other hand, the results of quantitation of the HCV core antibody titer were closely associated with the presence of HCV RNA using core protein with the recombinant vaccinia expression system or recombinant E. coli system (JCC-2). Especially, in the group of high responders to interferon treatment, the antibody titer against core protein was apparently decreased after the end of interferon therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Summary and evaluation of genome and antibody diagnosis in hepatitis C virus infection]. 753 27

Techniques of enzyme-linked immunosorbent assay based on synthetic multiple peptide fragments and second generation recombinant immunoblot assay (RIBA) were used to study the patterns of specific antibody response in 10 cases of posttransfusion hepatitis (PTH) during a period of 36-38 weeks after blood transfusion. Nine cases were positive with serum anti-HCV, including 8 cases positive with serum HCV-RNA. Antibodies to core protein of HCV showed a higher positive rate and were detected 1-3 weeks earlier than those to the putative nonstructural (NS) protein. Anti-HCV IgM to core protein were detected 1-4 weeks earlier than anti-HCV IgG and the detective absorbent values of anti-HCV IgM were positively correlated with the levels of serum ALT (P < 0.01). "Passive transfer" of anti-HCV were found in 3 cases. These facts suggest that HCV is the major causative agent of PTH cases in our district and anti-HCV IgM to core protein is a putative serological marker not only for early diagnosis of HCV infection but also for demonstration of active HCV infection.
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PMID:[A study on the patterns of early specific antibody response in patients with posttransfusion hepatitis C]. 753 48

We have defined 10 linear immunogenic regions encoded by the putative hepatitis C virus (HCV) structural proteins (core and envelope) by employing an enzyme-linked immunosorbent assay (ELISA) and by using 17 sequential synthetic peptides covering the N-terminal 330 amino acids of the structural polyproteins as antigens. These peptides correspond to amino acids 1 to 24, 21 to 44, 42 to 68, 64 to 91, and 100 to 120 of the putative core protein and amino acids 192 to 212, 223 to 238, 236 to 258, 250 to 266, and 307 to 330 of the putative envelope protein. In particular, the peptide covering amino acids 21 to 44 of the core protein was reactive with all but one (40 of 41) of the serum samples giving a positive signal in the passive hemagglutination assay (PHA) using the core and nonstructural proteins (NS 3/4) of the virus as antigens. We detected the HCV genome in 25 (61%) of 41 PHA-positive serum samples by the polymerase chain reaction (PCR) test. Of 25 PCR-positive serum samples, 17 serum samples had reactivity to the peptides derived from the envelope protein. On the other hand, only 1 of the 16 PCR-negative serum samples had reactivity to the peptides derived from the envelope protein. Interestingly, we often observed high serum alanine aminotransferase levels in PCR-positive individuals bearing antibodies to the envelope protein.
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PMID:Detection of antibodies to hepatitis C virus (HCV) structural proteins in anti-HCV-positive sera by an enzyme-linked immunosorbent assay using synthetic peptides as antigens. 768 49

We evaluated the clinical significance of the antibody to hepatitis C core protein (anti-p22) analysing 147 sera from 99 patients; 45 of them had post-transfusion non A non B (NANB) hepatitis, 28 cryptogenic non A non B hepatitis, 12 chronic hepatitis B, 7 chronic hepatitis D, 6 other forms of liver disease (4 primary biliary cirrhosis, 2 autoimmune hepatitis) and 1 rheumatoid arthritis. All sera were tested by commercial 1st and 2nd-generation ELISAs and anti-p22 single antibody ELISA. We found a highly significant correspondence between anti-p22 and commercial assays (p = 0.0001). HCV-RNA was detected by reverse transcriptase polymerase chain reaction (RT-PCR) in sera showing positive or negative concordant results and in all sera (24) that showed discordant results by anti-p22 and commercial ELISAs. HCV-RNA was found in 14 of 17 (82%) anti-p22 positive sera that were negative by commercial ELISAs, in 1 of 7 (14.3%) anti-p22 negative sera that were positive by commercial ELISAs (p = 0.001) and in all control sera from patients with positive concordant results. It was undetectable in 7 sera from patients with autoimmune diseases (negative by all ELISAs). We studied follow-up sera from 16 patients treated with interferon: 8 long-term responders (with persistently normal ALT levels for at least 24 months after discontinuation of therapy and histological remission) and 8 non-responders. Sera were also tested by a 4-antigen recombinant immunoblotting assay (RIBA II).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical significance of the antibody to the putative core protein of hepatitis C virus in patients with chronic liver disease. 769 Aug 74

We previously developed a method for introducing foreign genes into liver tissue using liposomes with incorporated hemagglutinating virus of Japan (HVJ, Sendai virus), and found that liver cells transfected with the E. coli beta-galactosidase gene or the gene for hepatitis B virus (HBV) surface protein (HBsAg) expressed these proteins in vivo. Here, we analyzed cellular reactions leading to hepatitis in the liver by expressing the genes of HBV in vivo. Lymphocytes were eluted directly from liver transfected with the HBsAg genes and shown to be cytotoxic only to cells expressing HBsAg in vitro. These lymphocytes were identified as cytotoxic T lymphocytes with the CD4- CD8+ phenotype. Transfer of these lymphocytes to transgenic mice with the whole HBV genome led to elevation of the serum glutamic-pyruvic transaminase (SGPT) level, indicating the induction of hepatitis due to the cytotoxic T lymphocytes in vivo. Similarly, direct transfer of the gene for the HBV secretory core protein (HBeAg) induced expression of HBeAg in hepatocytes and the appearance of antibody against HBeAg in the serum. However, using this system, we found that the lymphocytes infiltrating the transfected liver showed no cytotoxicity specific for HBeAg. These results indicate that expression of HBsAg, one of the components of virions, in animal liver induced hepatitis efficiently through generation of specific cytotoxic T lymphocytes (CTL) without any expression of the other viral components. This in vivo experimental system should be useful for evaluating how expression of a given gene induces cellular reactions and intrinsic functions in the living body.
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PMID:Use of the hemagglutinating virus of Japan (HVJ)-liposome method for analysis of infiltrating lymphocytes induced by hepatitis B virus gene expression in liver tissue. 839 62

We previously reported that interferon-gamma (IFN-gamma) production by PBMC in response to HCV core protein was increased in patients with type C chronic liver disease. To understand better the pathophysiology of this disease, we evaluated production of IL-10 and IL-12 by PBMC from 41 patients with chronic HCV infection, including asymptomatic HCV carriers with persistently normal serum ALT values. IL-10 is known to inhibit many effector functions of the immune system, suppressing Th1-type cell development, while IL-12 stimulates differentiation of Th1-type cells, facilitating cell-mediated immunity. IL-10 production was determined by culturing lymphocytes with concanavalin A (Con A), while IL-12 was produced by monocytes in the presence of Staphylococcus aureus Cowan 1 (SAC) with or without recombinant HCV core protein, respectively. The cytokine levels in culture supernatants were measured by ELISA. Spontaneous IL-10 production was greater in patients with chronic hepatitis (CH) (229 +/- 119 pg/ml, P < 0.01) and liver cirrhosis (LC) (185 +/- 88 pg/ml, P < 0.05) than in controls (119 +/- 27 pg/ml), while it was decreased during IFN treatment (70 +/- 25 pg/ml). Both HCV core protein and Con A enhanced IL-10 production by cells from HCV-infected patients. IL-12 was not detectable in medium alone cultures, and SAC-induced IL-12 production did not differ between various patient groups and controls. Simultaneous addition of HCV protein resulted in an increase of IL-12 production in chronic liver disease compared with SAC-alone cultures. Addition of IL-10 to the cultures equally suppressed IFN-gamma production for both controls and patient groups, but the enhancing effect of IL-12 on IFN-gamma production was significantly less in LC than in controls and other patient groups. The findings suggest that secretion of IL-10/IL-12 by cells from control individuals and various patient groups may be different, and that the cytokines might show different effects on IFN-gamma production by some cells.
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PMID:Production of interleukins 10 and 12 by peripheral blood mononuclear cells (PBMC) in chronic hepatitis C virus (HCV) infection. 909 22

We retrospectively assessed the frequency and clinicopathologic and virologic significance of production of immunoglobulin M (IgM) antibody to hepatitis C virus (HCV) core protein in patients with chronic hepatitis C. Sera from 60 patients with chronic hepatitis C were tested for IgM anti-HCVcore (anti-HCc). Twenty of these patients received ribavirin plus interferon-alpha for 24 weeks, and were classified as sustained, transient, or nonresponders on the basis of alanine aminotransferase levels and the presence of HCV RNA at the end of treatment and 24 weeks later. IgM anti-HCc was detected in 21 patients. There was no correlation between the presence of IgM anti-HCc and clinical features such as sex, age, mode of transmission, serum levels of alanine aminotransferase, HCV genotype, serum HCV titer, or histologic findings. Among the patients who received ribavirin plus interferon-alpha, the mean IgM anti-HCc level before therapy was comparable between sustained (n = 10), transient (n = 8), and nonresponders (n = 2). A statistically significant decrease in IgM anti-HCc response during antiviral therapy was observed in the 18 responders who became negative for serum HCV RNA at the end of therapy. These data suggest that IgM anti-HCc is of limited clinical usefulness as a marker of chronic HCV infection. Serial testing for IgM anti-HCc may provide a marker of antiviral response.
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PMID:Immunoglobulin M antibody response to hepatitis C virus core protein in patients with chronic hepatitis C. 934 83

Fifteen kidney transplant recipients with chronic hepatitis C were given 3 million units recombinant alpha2b-interferon for 142+/-35 days. There were significant decreases in hepatitis C virus (HCV) RNA 1 month after the initiation of treatment (p < 0.01), and at the end of treatment (p < 0.05). HCV RNA was undetectable by PCR analysis during treatment in 5 patients. But HCV RNA reappeared in all patients 1 month after the cessation of therapy, and the level of viremia returned to baseline. While all patients had normalized alanine aminotransferase (ALT) activities at the end of therapy, 11 experienced a relapse during the follow-up period (1 year). There was a correlation between the amount of HCV RNA at the end of treatment and the time of relapse. Serum IgM against core protein of HCV were detected in 7/15 patients. Anti-core IgM remained detectable during treatment and afterwards. There was no correlation between IgM status and other virological parameters, or ALT activity.
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PMID:Kinetics of HCV viremia in kidney transplant recipients during and after alpha-interferon therapy. 938 58


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