Interferon type I gene expression in chronic hepatitis C View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2004-09

AUTHORS

Sabine Mihm, Michael Frese, Volker Meier, Perdita Wietzke-Braun, Jens-Gerd Scharf, Ralf Bartenschlager, Giuliano Ramadori

ABSTRACT

Hepatitis C virus (HCV) frequently causes chronic liver disease. The cause of viral persistence might be an inappropriate type I interferon (IFN) induction. To analyze the host's IFN response in chronic hepatitis C, we measured the transcription level of type I IFN genes as well as type I IFN-regulated genes in liver tissue and corresponding blood samples from patients with chronic hepatitis C, nonviral liver diseases, and a suspected but later excluded liver disease. Competitive and real-time RT-PCR assays were used to quantify the messenger RNA (mRNA) levels of all known IFN-alpha, IFN-beta, and IFN-lambda genes and those of some IFN-regulated genes. We failed to detect any hepatic type I IFN mRNA induction, although liver tissue of chronic hepatitis C patients contained high numbers of some type I IFN-inducible effector mRNA molecules. Analysis of peripheral blood samples, however, showed a clear type I IFN induction. Parallel experiments employing HCV replicon cell lines revealed that replication of HCV RNA is not sufficient to induce any type I IFN nor to induce directly type I IFN-regulated genes such as MxA. In conclusion, our data provide evidence for the absence of an induction of type I IFN genes by HCV in the human liver and argue for a further development of type I IFN-based therapies. More... »

PAGES

3700135

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/labinvest.3700135

DOI

http://dx.doi.org/10.1038/labinvest.3700135

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1004800167

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/15208644


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