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:2.7.7.49 (reverse transcriptase)
31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The relative value of an anti-hepatitis C virus (HCV) serological assay and reverse transcriptase-nested polymerase chain reaction assays (RT-PCR) were investigated for the constant 5' putative noncoding region of HCV for the diagnosis of HCV-associated chronic liver diseases in India. One hundred fifteen patients with biopsy proven chronic active hepatitis and 140 cases of cirrhosis of the liver were investigated for anti-HCV antibody using a second generation commercial enzyme-linked immunosorbent assay (ELISA). A proportion of these patients: 42 with chronic hepatitis and 27 with cirrhosis of the liver were analysed further for HCV RNA in the serum using RT-nested PCR assay. Thirty-three (12.9%) of the 255 patients were positive for anti-HCV antibody and 23 of 69 (33.3%) patients were positive for HCV RNA in serum. Fifteen of the 33 (45.5%) anti-HCV positive patients had HCV RNA in the serum. Eight of 36 (22.2%) HCV seronegative patients tested were found with HCV RNA. This indicates that the diagnosis of HCV infection is not possible if it is based solely on the available serodiagnostic tests. Inclusion of both assays improved the diagnostic efficiency, 18.8% (13/69) were negative for all virological markers associated with HBV and HCV infection. Since a majority of the chronic liver disease patients (143/255 [56%]) were seronegative for either HBV or HCV infection, it is significant that HCV RNA was detected in 38% (8/21) of a randomly selected group from these patients. The antibody assay and PCR were compared using interclass correlation (kappa statistics).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diagnosis of hepatitis C virus-associated chronic liver disease in India: comparison of HCV antibody assay with a polymerase chain reaction for the 5' noncoding region. 753 53

The purpose of this study was to compare the serological analysis for hepatitis C infection using the recombinant immunoblot assay (RIBA) to the direct in situ localization of the hepatitis C viral genome using the reverse transcriptase (RT) in situ PCR technique. Concurrent sera and liver biopsies from 42 patients with clinical and histologic evidence of chronic liver disease were studied. Antibodies against hepatitis C specific antigens were demonstrated by RIBA in the sera of 39/42 (92%), and PCR amplified viral cDNA was detected in the biopsies of 21 (54%) of the 39 seropositive patients. The detection rate using standard in situ hybridization for the tissues known to be viral positive with RT in situ PCR was 9/21 (42%). It is concluded that approximately one-half of patients with chronic hepatitis and serologic evidence of hepatitis C infection will not have virus detectable in their liver biopsy even with a highly sensitive PCR-based technique.
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PMID:Comparison of serologic analysis and in situ localization of PCR-amplified cDNA for the diagnosis of hepatitis C infection. 755

Hepatocyte growth factor (HGF) and transforming growth factor alpha (TGF-alpha) stimulate liver regeneration, whereas transforming growth factor beta 1 (TGF-beta 1) inhibits it in rats. However their significance in human liver diseases, especially in severe acute liver injury, remains unclear. We studied HGF, TGF-alpha, and TGF-beta 1 messenger RNA (mRNA) expression in the livers of patients with live diseases using a competitive reverse transcriptase polymerase chain reaction. As little as a twofold difference in mRNA expression could be detected from minute liver biopsy samples. We then examined cell proliferation using proliferating cell nuclear antigen (PCNA) staining. HGF mRNA levels were significantly higher (approximately threefold) in acute hepatitis (AH) than in exacerbation of chronic liver disease (EX) (P < .05). TGF-alpha mRNA levels were significantly greater in AH (approximately twofold) than EX (P < .05), and the levels were significantly higher (approximately threefold) in chronic hepatitis (CH) than in EX (P < .05). The TGF-beta 1 mRNA levels in all the groups were not significantly different. In acute liver injury (AH and EX), there was a significant correlation between HGF mRNA expression and the PCNA labeling index (LI) in the liver (r = .87, P < .005). TGF-alpha mRNA expression also correlated with the PCNA LI (r = .92,P < .0001). There was no significant correlation between the serum HGF and the PCNA LI in the liver. In conclusion, HGF and TGF-alpha produced in the liver stimulate hepatocyte proliferation in response to acute liver injury in humans.
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PMID:Expression of hepatocyte growth factor, transforming growth factor alpha, and transforming growth factor beta 1 messenger RNA in various human liver diseases and correlation with hepatocyte proliferation. 869 Apr

Hepatitis C Virus (HCV) is the major cause of parentally transmitted non-A, non-B hepatitis. We studied the incidence of HCV Viremia in blood donors, hemophiliacs and patients with chronic liver disease who are positive for antibodies to HCV, and then correlated the HCV genotypes among the three groups. 23 blood donors, 10 hemophiliacs and 97 patients with chronic liver disease were found to be positive for anti-HCV during this study period from June 1993 to December 1993. Only 3 (13%) blood donors, 6 (60%) hemophiliacs and 71 (73%) patients with chronic liver disease were found to be viremic when tested for HCV RNA by reverse transcriptase-polymerase chain reaction (RT-PCR). The low incidence of viremia among blood donors may be due to any one of the following three reasons. 1, the level of viremia was below the level of detection. 2, the viremia was intermittent with persistent infection. 3, the majority of cases represented resolved infection. The HCV genotypes were heterogeneous among the three groups. All the blood donors with viremia and 35 (50%) of patients with chronic liver disease, belonged to type II (1b). However only one (17%) of the hemophiliacs belonged to type II (1b). Studies have shown that the genotype I(1a) is the predominant type in the USA and Europe, whereas type II(1b) is more frequent in the Far East. It is also suggested that type II (1b) is associated with non-responsiveness to interferon therapy. Our hemophiliacs were treated with imported coagulation factors, thus they were probably exposed to the genotypes in the west. There was significant difference in the incidence of HCV type II (1b) among local blood donors and hemophiliacs (P = 0.005). However the difference between the hemophiliacs and the patients with chronic liver disease was not statistically significant. The number of patients in this study was too small to draw any firm conclusions. However the findings highlight the importance of studying the genotypes of patients with Hepatitis C infection due to their relevance in the management of these cases with interferon therapy.
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PMID:The incidence of viremia and the heterogeneity of hepatitis C virus genotypes among blood donors, hemophiliacs and patients with chronic liver disease. 900 55

Hepatitis G virus (HGV) is a recently described, parenterally spread, positive-strand RNA virus of the Flaviviridae family. There is a high rate of HGV coinfection in patients with hepatitis C virus (HCV). Whether HGV can cause or is pathogenetically related to clinically apparent chronic liver disease, or whether HGV alters the course of hepatitis C in patients who are coinfected with both viruses is unknown. We studied 13 biopsy specimens from 11 patients coinfected with HGV and HCV and compared them with 15 biopsy specimens from a group of patients infected only with HCV who were matched for age, sex, disease duration, and transmission mode to characterize the histologic features of coinfected liver biopsy specimens and to look for any histologic features that might allow identification of coinfected patients. Three of the biopsy specimens from coinfected patients had a modified histologic activity index score of minimal chronic hepatitis, three of mild, two of mild/moderate, and five of moderate chronic hepatitis. Bile duct injury was absent in seven specimens, minimal in five, and mild in one. The biopsy specimens from patients who were coinfected with HGV and HCV had similar histologic features to the biopsy specimens of patients infected with HCV alone. There were no detectable histologic differences between the biopsy specimens from the two patient groups. The P values for the statistical comparisons confirmed this impression. In addition, no group of histologic features distinguished the coinfected patient group from the control group. Any suspicion that a clinician might have about the presence of HGV requires confirmation by reverse transcriptase-polymerase chain reaction testing of serum samples. Our results suggest that HGV most likely does not actively participate in the cytotoxic effects of chronic hepatitis or does so by a mechanism as yet undefined. Although HGV can cause chronic infection, the present study provides no evidence that it causes or contributes to chronic hepatitis.
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PMID:Comparative histologic features of liver biopsy specimens from patients coinfected with hepatitis G and C viruses with chronic hepatitis C virus alone: an age-, sex-, disease duration-, and transmission-matched controlled study of chronic hepatitis. 938 41

Increasing evidence suggests that the hepatitis C virus (HCV) might be involved in the pathogenesis of B cell non-Hodgkin's lymphomas (NHL). Since several HCV genotypes are currently identifiable and might be involved in the pathogenesis of different diseases (with different severity and responsiveness to therapy), the aim of our study was to assess the prevalence of viral genotypes in a group of patients with HCV-related NHL. Among 470 consecutive patients, 42 HCV Ab-positive cases were identified. HCV RNA could be detected by reverse transcriptase-polymerase chain reaction and genotyping performed in 31 of these cases. As compared to our control group (211 healthy blood donors and patients with chronic liver disease), a striking high prevalence of genotype 2ac was detected among B cell NHL (48.4 vs 9.0%), with a relative risk of infection of 5.37 (P < 0.0001). No major differences were observed in the distribution of NHL histotypes and in the clinical features among patients with genotype 1b (the other most frequent genotype) or 2ac, a part from a trend towards a higher percentage of liver disease and a lower likelihood of response to interferon for patients with genotype 1b. The same high prevalence of genotype 2ac has been recently reported in patients with mixed cryoglobulinemia (MC), monoclonal gammopathies, B cell NHL complicating MC and autoimmune hepatitis. All these data taken together suggest that genotype 2ac might be involved in the pathogenesis of lymphoproliferative and autoimmune disorders.
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PMID:The genotype of the hepatitis C virus in patients with HCV-related B cell non-Hodgkin's lymphoma. 944 35

Hepatitis G virus (HGV) is a flavivirus that can cause acute hepatitis and persistent infection but its role in chronic liver disease or primary liver cancer is unproven. In this study we have examined the prevalence of HGV RNA in the serum of patients with hepatitis C virus (HCV) infection and in patients with cryptogenic chronic liver disease, including non-alcoholic steatohepatitis (NASH), and in patients with HCV-related hepatocellular carcinoma (HCC) and HCC arising in patients with cryptogenic liver disease. One-hundred and thirty patients who were positive for antibody to HCV (anti-HCV), 54 patients with cryptogenic chronic liver disease (including 17 patients with NASH) and 46 patients with hepatitis C-related (n = 27) or cryptogenic liver disease-related HCC (n = 19) were studied. HGV RNA was detected using nested reverse transcriptase-polymerase chain reaction (RT-PCR) and was found in 16.1% of patients with HCV infection. HGV RNA was not detected in any patient with cryptogenic liver disease. In patients with HCC, 7/34 samples were positive for HGV RNA and six out of seven HGV-positive subjects also had HCV infection. Only one patient with HCC in cryptogenic liver disease was positive for HGV RNA. Hence, cryptogenic liver disease in the UK is not caused by HGV/GBVc infection. It seems unlikely that HGV plays a significant role in hepatocarcinogenesis.
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PMID:Hepatitis G infection: role in cryptogenic chronic liver disease and primary liver cell cancer in the UK. Trent Hepatitis C virus Study Group. 965 69

In situ reverse transcriptase-polymerase chain reaction is a novel and exciting technique which couples the extremely high sensitivity of DNA amplification with the advantages of in situ hybridisation, allowing the preservation of cell morphology and the localisation of the positive signal within intact cells. In this brief report, we analyse and discuss the application of such a technique to the study of hepatitis C virus (HCV) infection, the most common cause of chronic liver disease worldwide. Moreover, given the lymphotropism of this virus, we describe here our own approach to detect and localise HCV RNA within intact peripheral blood mononuclear cells and to quantify the relative number of infected cells.
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PMID:In situ reverse transcriptase-polymerase chain reaction: an innovative tool for hepatitis C virus RNA detection and localisation, and for quantification of infected cells. 972 90

Telomerase is a specialized type of reverse transcriptase that catalyzes the synthesis and extension of telomeric DNA. High levels of telomerase activity have been detected in most hepatocellular carcinoma (HCC) tissues; very weak telomerase activity is, however, detected in approximately half of nontumorous chronic liver disease tissues. The purpose of this study was to investigate the possible source of this weak telomerase activity in these tissues using quantitative competitive reverse transcription (RT)-polymerase chain reaction (PCR) and in situ RT-PCR. Competitive RT-PCR indicated that the relative amount of human telomerase RNA (hTR) was significantly higher in chronic hepatitis or liver cirrhosis compared with the normal liver (p < 0.005), and in HCC compared with the normal liver (p < 0.001) and with chronic hepatitis or liver cirrhosis (p < 0.0001). In the normal liver tissue, hTR was detected by in situ RT-PCR in occasional sinusoidal cells and nuclei of occasional hepatocytes. In tumor-free liver or tumor-bearing liver, hTR was detected in sinusoidal cells, infiltrating lymphocytes, occasional proliferative bile ductal epithelial cells, and the nuclei of occasional hepatocytes. In HCC, hTR was detected in nuclei of all HCC cells as an intense signal and in sinusoidal cells. These results indicate that the amount of hTR increases in the nuclei of hepatocytes during hepatocarcinogenesis, and that the cells associated with the weak telomerase activity in approximately half of the nontumorous chronic liver lesions are mainly migrating lymphocytes and sinusoidal cells.
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PMID:Quantitative analysis and in situ localization of human telomerase RNA in chronic liver disease and hepatocellular carcinoma. 995 7

We previously demonstrated that whole blood contains significantly more hepatitis C virus (HCV) RNA than plasma. To validate the whole-blood-based HCV RNA detection method, a prospective comparison of HCV RNA detection in whole blood and plasma from 50 patients with chronic liver disease was undertaken. Whole-blood and plasma aliquots were independently tested for HCV RNA by reverse transcriptase (RT) PCR assay, and plasma was tested by the Roche Amplicor assay. HCV RNA was detected in 35 of 50 (70%) whole-blood samples by RT-PCR but in only 26 of 50 (52%) plasma samples tested by the Amplicor assay (P < 0.01). HCV RNA was detected in 85% of HCV antibody-positive patients by the whole-blood method compared with 74% of plasma samples by the Amplicor method. The five HCV antibody-positive subjects who were negative by whole-blood-based RT-PCR assay were all receiving interferon therapy and had normal transaminases at the time of testing. HCV RNA was detected in 38% of HCV antibody-negative subjects by the whole-blood-based RT-PCR assay compared with 6.25% of these patients by the Amplicor assay (P < 0. 05). There were nine samples in which HCV RNA was detected in whole blood but the Amplicor test was negative. Eight of the nine RNAs prepared from these whole-blood samples tested positive in the Amplicor assay, thus confirming the specificity of our results. This study demonstrates that whole-blood-based HCV RNA detection is more sensitive than currently available commercial tests and that whole-blood RNA is suitable for use in commercial assays.
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PMID:Prospective comparison of whole-blood- and plasma-based hepatitis C virus RNA detection systems: improved detection using whole blood as the source of viral RNA. 998


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