標題: Hepatic expression of MxA and OAS1 in an ex vivo liver slice assay independently predicts treatment outcomes in chronic hepatitis C
作者: Cheng, J. -C.
Yeh, Y. -J.
Huang, Y. -H.
Liang, K. -H.
Chang, M. -L.
Lin, C. -Y.
Yeh, C. -T.
生物資訊及系統生物研究所
Institude of Bioinformatics and Systems Biology
關鍵字: End of therapy response;interferon-stimulated gene;sustained virological response
公開日期: 1-二月-2012
摘要: . Antiviral effect of interferon is mediated by the expression of interferon-stimulated genes (ISGs). However, because of the difficulty in obtaining paired liver biopsies before and after interferon treatment, the key ISGs expressed in human hepatocytes and responsible for interferon-based antiviral activities in chronic hepatitis C remain illusive. Prior to a standard course of peginterferon plus ribavirin therapy, 104 patients underwent a liver biopsy. A small piece of the liver biopsy sample from each patient was submitted for ex vivo tissue culture in the presence or absence of interferon. Hepatic expression of 8 ISGs was detected by RT-PCR. The ISG expression patterns and clinicopathological variables were correlated with subsequent treatment outcomes. Multivariate logistic regression analysis showed that hepatic MxA expression (P = 0.008) and leucocyte count (P = 0.040) independently predicted the end of therapeutic virological response, while hepatic OAS1 expression (P = 0.003), genotype 1 (P = 0.002), HCV-RNA level (P = 0.007), AST/ALT ratio (P = 0.004) and leucocyte count (P = 0.034) independently predicted the sustained virological response. Immunohistochemistry analysis showed that interferon-induced OAS1 expression localized to the hepatocytes. In conclusion, hepatic MxA and OAS1 expression predicted, respectively, the end of therapeutic and sustained virological responses in interferon-based treatment of chronic hepatitis C.
URI: http://dx.doi.org/10.1111/j.1365-2893.2011.01538.x
http://hdl.handle.net/11536/15242
ISSN: 1352-0504
DOI: 10.1111/j.1365-2893.2011.01538.x
期刊: JOURNAL OF VIRAL HEPATITIS
Volume: 19
Issue: 2
起始頁: E154
結束頁: E162
顯示於類別:期刊論文


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