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)

A nonisotopic in situ hybridization (NISH) assay was used to detect hepatitis C virus (HCV) RNA. A synthetic oligonucleotide complementary to bases 252-301 of the highly conserved 5' noncoding region of the HCV genome was end-labeled by terminal deoxynucleotidyltransferase using digoxigenin-conjugated dUTP. The hybridized oligomer was revealed by an immunohistochemical reaction after incubation with an alkaline phosphatase-conjugated anti-digoxigenin antibody and subsequent amplification with a complex of alkaline phosphatase and anti-alkaline phosphatase antibodies. The intracellular distribution of HCV RNA was monitored in the livers of two chimpanzees experimentally infected with the H strain of HCV and compared with the serum alanine aminotransferase activity, serum HCV RNA, and liver histopathology. Most cells were stained in the cytoplasm as early as 2 days after inoculation, 1 and 2 days, respectively, before the appearance of viral RNA in the serum. The time course of HCV RNA replication was correlated with increases in serum alanine aminotransferase. However, neither one paralleled the appearance of liver cell necrosis nor showed any correlation with the inflammatory response. The NISH signal was not found in liver biopsy specimens taken from these two animals before inoculation with HCV, from chimpanzees with acute hepatitis type A, B, or delta, or from two animals never experimentally infected with any hepatitis agent; moreover, it disappeared when the positive specimens were predigested with RNase and it was not observed after hybridization of positive controls with a labeled oligomer unrelated to HCV RNA. Thus, detection of liver HCV RNA by NISH is a sensitive and specific method for studying HCV replication at the cellular level. Intracellular replication of HCV did not appear to be associated with histopathologic changes in the liver, although the correlation with increases of liver enzyme activity in the serum suggested possible damage to the liver cell membrane.
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PMID:Detection of intrahepatic replication of hepatitis C virus RNA by in situ hybridization and comparison with histopathology. 131 16

Serial serum samples from cardiac patients with a history of chronic or resolved post-transfusion non-A, non-B hepatitis were analyzed by a combination of cDNA synthesis and the polymerase chain reaction (cDNA/PCR) to amplify HCV RNA. Analysis of sera drawn after the acute hepatitis episode from 8 of the patients who had an acute, resolving HCV infection showed no detectable levels of HCV RNA when primers from the NS3 region were used. Evaluation of these sera with primers from the 5'-untranslated (5'-UT) region revealed that one patient was positive for HCV RNA. Further analysis of serial serum samples available from two of these patients indicated that a resolved infection was associated with a disappearance of detectable HCV RNA after a peak level during the acute phase of the disease. In contrast, post-acute samples from 4 of 6 patients with symptomatic acute HCV infection evolving to chronicity were positive for HCV RNA using primers from the NS3 region, however, upon retesting with primers from the 5'-UT region, all 6 patients were found to be positive. Analysis of serial serum samples from 2 of these patients showed the persistence of HCV RNA in 70% of the samples. These two patients were subsequently treated with interferon alpha-2b. One patient resolved his disease and normalized his aminotransferase level during treatment and thereafter, while the other relapsed upon cessation of treatment. In these two patients, normalization of ALT levels was consistent with the absence of HCV RNA while relapse of disease was confirmed by the reappearance of detectable levels of HCV RNA. These results indicate the utility of HCV RNA as a marker for persisting HCV viremia and in differentiating patients with ongoing active HCV infection from those with an acute resolving disease.
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PMID:Detection of hepatitis C viral RNA by the polymerase chain reaction in serum of patients with post-transfusion non-A, non-B hepatitis. 131 77

Three hundred and eighty-seven chronic hemodialysis patients were evaluated, in a multicenter study, to investigate the epidemiology of hepatitis C virus. In anti-HCV seropositive patients, serum ALT values and blood transfusions were retrospectively compared; blood donors were studied for serum transaminases. In seropositive patients without previous blood transfusions, analysis of dialysis schedule was done. Eventually, the intrafamilial transmission of hepatitis C virus was studied in 104 family members. The prevalence of HCV infection in hemodialysis patients was 15.7%. The incidence of acute hepatitis was frequent, while chronic hepatitis incidence was less than expected (17.5%). Intrafamilial diffusion was low (1.9%). Blood-transfusion-related infections seem to be negligible, while cross-contamination in dialysis units seems to be very important.
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PMID:Hepatitis C virus in dialysis units: a multicenter study. 132 77

In order to clear some aspects of HCV infection, we evaluated quarterly HCV markers by a RIBA 1 test (antigens c100-3 and 5.1.1) and monthly transaminases (ALT and AST) for 14 months in 89 HBsAg-free maintenance hemodialysis patients (MHP), and we retrospectively examined clinical records until the start of hemodialysis treatment. At the start of the study, 16 patients showed HCV antibodies (HCV+) and 73 were antibody-free (HCV-). 39 subjects of the staff were also examined. No HCV+ patient showed seroconversion, 10 showed irregular or persistent elevation of AST and ALT. In the retrospective evaluation 14 patients suffered from acute hepatitis (AH). Only 3 cases showed temporal relation with blood transfusions. In 1 case a 36-month temporary normalization of transaminases was noticed. 3 HCV-patients showed seroconversion (1 during AH), 13 showed severe or moderate elevations of transaminases. In the retrospective evaluation, 6 patients suffered from AH. All subjects of the staff were HCV- and showed no seroconversion or changes of transaminases. At the end of the study, we performed a RIBA 2 test containing the HCV antigens c100-3, 5.1.1, c22-3 and c33c. The 6 patients who suffered from AH showed at least 1 positivity for new proteins. Most of AH in MHP are likely due to HCV infection; besides transfusions, cross-infection during the dialytic procedure may be responsible for many cases of HCV infection; long-term normalization of transaminases may not secure against infectivity.
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PMID:Prospective and retrospective assessment of clinical and laboratory parameters in maintenance hemodialysis patients with and without HCV antibodies. 132 79

The incidence of HCV antibodies has been evaluated in 123 chronic hemodialysis (HD) patients (Group A; 55 M and 68 F) and in 37 consecutive HD patients (group B) admitted to our hospitals for acute hepatitis. In group A, HCV antibodies were present in 27% of the patients. 20 of 36 (55%) had previously received blood transfusions. 21 patients (58%) were also positive for HBV Ab. In 8 patients, ALT were significantly increased. In group B, the diagnosis of HCV-related acute hepatitis was made in 11 patients. 8 of them had previously received blood transfusions. Seroconversion occurred 2-3 months after onset of the disease.
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PMID:Hepatitis C virus-related acute and chronic hepatitis in hemodialysis patients. 132 81

The influence of viremia on hepatic injury in patients infected with hepatitis C virus was examined by analysis of the relationship between alanine aminotransferase activity and the amount of hepatitis C virus RNA in sequential serum samples from I untreated patient with acute hepatitis C and 3 untreated patients with chronic hepatitis C. Semiquantitative analysis by the competitive-reverse-transcription/polymerase-chain-reaction method indicated that the quantity of hepatitis C virus RNA in the serum affected the disease activities of acute and chronic hepatitis C through their natural clinical courses in all these patients. The nucleotide sequence encoding the putative envelope region of the viral genome in the patient with acute hepatitis C was examined. Blood samples taken serially at 2 times of exacerbation of the hepatitis revealed 2 nucleotide mutations, resulting in changes of predicted amino acid residues. This finding suggests that nucleotide mutations in the envelope region of the viral genome may be responsible for the recurrent hepatic injury attributed to recurrence of viremia in patients with hepatitis C. From these aspects, the serial divergence of the virus genome in infected individuals, especially in the region encoding the viral envelope protein, may possibly play an important role in developing chronic infection of hepatitis C virus.
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PMID:Correlation between the serum level of hepatitis C virus RNA and disease activities in acute and chronic hepatitis C. 133 Sep 30

Intercellular adhesion molecule-1, an immunoglobulin supergene family member, is known to account for important steps in cell activation and the immune response. By a non-isotopic slot-dot immunoblotting assay, we measured circulating levels of intercellular adhesion molecule-1 in 26 patients with hepatitis C virus-associated chronic active liver disease before and after beta-interferon therapy, in 6 patients with non-A, non-B acute self-limiting hepatitis and in 13 healthy subjects. Circulating intercellular adhesion molecule-1 was found in 10 of 13 (77%) normal controls at low concentrations which were not statistically different from those measured in patients with hepatitis C virus-associated chronic active liver disease responsive to beta-interferon, whereas significantly higher levels were found in unresponsive patients. Higher serum intercellular adhesion molecule-1 levels were found in 4 of 10 (40%) beta-interferon-responsive patients compared with 13 of 16 (18%) unresponsive patients. Intercellular adhesion molecule-1 levels persisted after discontinuation of beta-interferon treatment and did not correlate with hepatocytolysis (as indicated by alanine aminotransferase serum activity) either in chronic active liver disease or acute hepatitis. However, a good correlation was found between intercellular adhesion molecule-1 and its expression on liver cells, thus emphasizing that induced circulating levels may reflect the state of activation at the sites of the inflammatory process. These data strongly support the view that intercellular adhesion molecule-1 plays an important role in liver cell damage in hepatitis C virus-associated acute and chronic liver disease, and that its circulating levels may be a good prognostic parameter of responsiveness to beta-interferon therapy.
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PMID:Circulating levels and liver tissue distribution of intercellular adhesion molecule-1 during beta-interferon therapy of hepatitis C virus-associated chronic active liver disease. 135 8

The risk of developing a chronic carriage state after acute hepatitis B infection in adults was evaluated. Two hundred and eighty-nine HBV-susceptible heterosexual partners of acute hepatitis B patients were used to investigate the effectiveness of post-exposure immunoprophylaxis; 75 of them received hepatitis B vaccine, 72 hepatitis B hyperimmune globulin (HBIG), 71 vaccine plus HBIG and 71 placebo. Participants were interviewed, clinically examined and serum specimens were taken at 1, 3, 6 and 9 months after their first intervention. Serum samples were tested for ALT and HBV markers (HBsAg, anti-HBc and anti-HBs) using radio immunoassays. Forty-six (15.9%) of the heterosexual partners examined were infected; the incidence of HBV infections was higher among placebo (18.3%, 13/71) and HBIG (18.1%, 13/72) recipients compared to vaccine (16.0%, 12/75) and HBIG plus vaccine (11.3%, 8/71) recipients, but the differences were not statistically significant. Infections were significantly more often subclinical after immunoprophylaxis (p = 0.03). HBsAg was detected in all eight clinical and in 13 of the 38 subclinical cases. In the remaining 25 subclinical cases HBV infections were diagnosed by the development of anti-HBc and anti-HBs during the follow-up period. Finally, all 46 cases studied cleared the HBsAg.
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PMID:Chronic liver disease rarely follows acute hepatitis B in non-immunocompromised adults. 138 66

To assess the efficacy of interferon-alpha in acute hepatitis C, 28 patients with acute posttransfusion hepatitis were randomized to receive 3 million units of recombinant interferon-alpha three times weekly for 12 wk or no treatment. Biochemical, histological and serological parameters were monitored during 1 yr of follow-up. Serum ALT levels were normal at the end of therapy in 73% of treated patients and only in 38% of control patients (p = 0.06); these differences disappeared at 6 and 12 mo of follow-up. Anti-hepatitis C virus seroconversion occurred later and at a lower rate in the group of patients who received interferon-alpha. Treated patients had a trend toward less severe hepatic lesions with lower histological activity as compared with the control group, but no statistical differences were observed. No severe side effects of interferon-alpha were detected during the study. In summary, a 3-mo course of interferon-alpha in acute hepatitis C is safe and might have some effect in diminishing disease activity only during the treatment period; however, and probably because of a small sample size, no benefit of interferon-alpha in the long-term outcome of this disease was demonstrated.
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PMID:Interferon-alpha in acute posttransfusion hepatitis C: a randomized, controlled trial. 156 16

Cellular immunity to HBcAg was studied in hepatitis B virus carrier children and neonates born to hepatitis B virus carrier mothers. A significant proliferative response of peripheral blood mononuclear cells to HBcAg was found in 5 of 10 children with elevated ALT levels but in none of the nine HBeAg-positive children with normal ALT levels. HBeAg but not HBsAg was detected in cord blood of 9 of 10 neonates born to HBeAg-positive carrier mothers, suggesting exposure of these neonates to HBeAg in utero. However, cord mononuclear cells from neonates born to HBeAg-positive carrier mothers did not show a significant change in the proportion of suppressor and helper T-cell subsets or proliferative response to HBcAg. Nor did they produce interleukin-2 receptor after being cocultured with HBcAg. The unresponsiveness of peripheral-blood mononuclear cells or cord mononuclear cells to HBcAg was not reversed by CD8+ cell depletion. Although cord blood mononuclear cells from neonates born to carrier mothers positive for antibody to HBeAg also did not respond to HBcAg, we encountered an infant, born to a carrier mother positive for antibody to HBeAg, who contracted acute hepatitis B at 2.5 mo of age. The baby's peripheral-blood mononuclear cells showed a significant proliferative response to HBcAg. These results support the view that transplacental maternal HBeAg probably induces a specific unresponsiveness of helper T cells to HBcAg and HBeAg in the neonates born to HBeAg-positive carrier mothers. This specific helper T cell tolerance could be maintained throughout the early replicative phase of carrier state but might break someday with the appearance of raised ALT level.
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PMID:Cellular immune response to HBcAg in mother-to-infant transmission of hepatitis B virus. 156 17


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