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Introduction: The pathogenesis of chronic hepatitis B depends on both, the immune response and oxidative stress. Aim of the study: To assess the hepatic expression of miR-122 and the antioxidant genes: HMOX-1, NQO1 and GFER1, in liver biopsy specimens obtained from patients with chronic hepatitis B, with regard to selected clinical and histological parameters, using RT-PCR. Results: The study group comprised 34 HBV-infected patients. Statistically significant associations were found between lower hepatic expression of HMOX-1 and greater severity of liver inflammation (p=0.04). However, significantly higher expression of NQO1 was observed in patients with advanced liver fibrosis (p=0.035). Hepatic expression of miR-122 in HBV patients was not associated with viral load or liver injury. Conclusion: The hepatic expression of HMOX-1and NQO1 may be associated with liver injuries in chronic hepatitis B. However, hepatic expression of miR-122 does not seem to correspond to progression of the liver disease.
EN
TT virus (TTV) was suggested to be the etiologic agent for non A-E hepatitis but this could not yet be proven due to high detection rates not only in hepatitis but also in healthy persons and sensitivity differences of PCR methods employed. The aim of this study was to evaluate TTV DNA positivity in non A-E hepatitis cases, chronic HBV and HCV hepatitis cases and healthy blood donors via PCR systems that target all regions of the viral genome used for viral detection. 23 non A-E hepatitis, 28 chronic HCV, 21 chronic HBV cases and 56 healthy blood donors were included in the study and evaluated by PCR protocols that target 5′-UTR, 3′-UTR and N22 (ORF1) regions. As a result, 3′-UTR and 5′-UTR PCR had comparable detection rates that were higher than N22 PCR. Differences in detection rates among study groups were not statistically significant for any PCR method. Hepatic enzyme levels of the patients were not correlated with the presence of TTV DNA. Detection rate was significantly higher for Non A-E hepatitis group when positivity rates from all methods were combined. These results suggest an alteration of viral genotypes in Non A-E hepatitis which might be associated with pathogenesis.
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