Ontology type: schema:ScholarlyArticle Open Access: True
2012-12
AUTHORSMohammed Asmal, Michael Seaman, Wenyu Lin, Raymond T Chung, Norman L Letvin, Ralf Geiben-Lynn
ABSTRACTBACKGROUND: Although there have been dramatic strides made recently in the treatment of chronic hepatitis C virus infection, interferon-α based therapy remains challenging for certain populations, including those with unfavorable IL28B genotypes, psychiatric co-morbidity, HIV co-infection, and decompensated liver disease. We have recently shown that ATIII, a serine protease inhibitor (serpin), has broad antiviral properties. RESULTS: We now show that ATIII is capable of inhibiting HCV in the OR6 replicon model at micromolar concentrations. At a mechanistic level using gene-expression arrays, we found that ATIII treatment down-regulated multiple host cell signal transduction factors involved in the pathogenesis of cirrhosis and hepatocellular carcinoma, including Jun, Myc and BMP2. Using a protein interactive network analysis we found that changes in gene-expression caused by ATIII were dependent on three nodes previously implicated in HCV disease progression or HCV replication: NFκB, P38 MAPK, and ERK1/2. CONCLUSIONS: Our findings suggest that ATIII stimulates a novel innate antiviral host cell defense different from current treatment options. More... »
PAGES226
http://scigraph.springernature.com/pub.10.1186/1743-422x-9-226
DOIhttp://dx.doi.org/10.1186/1743-422x-9-226
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PUBMEDhttps://www.ncbi.nlm.nih.gov/pubmed/23031791
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