[In this report, using a HCV subgenomic replicon cell culture system, we show that (1) long-term IFN stimulation can select cells defective for Stat3 activation, and the defect appears to be responsible for HCV IFN resistance in cell culture, (2) HCV subgenomic sequence mutations associated with long-term culture do not appear to be responsible for IFN resistance, (3) expression of the activated Stat3 reverses IFN resistance while a dominant negative form of Stat3 renders an IFN-sensitive cell line resistant to IFN, and (4) the IFN-resistant cell line exhibits enhanced suppressor of cytokine signaling 3 (SOCS3) expression in response to IFN stimulation, and blocking SOCS3 in the IFN-resistant cell line partially restores IFN sensitivity.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine.
Gene-disease associations inferred from text-mining the literature.
DisGeNET evidence - LITERATURE