Expression of intracellular interferon constitutively activates ISGF3 and confers resistance to EMC viral infection

Michael N. Rutherford, Aseem Kumar, Benoit Coulombe, Daniel Skup, David H. Carver, Bryan R.G. Williams

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The mechanism(s) by which interferon (IFN)-α confers resistance to viruses is currently being characterized. Previous studies have shown that binding of IFN-α to its high-affinity receptor activates transcription factor interferon-stimulated gene factor 3 (ISGF3), which positively regulates a number of antiviral genes including 2'-5'-oligoadenylate synthetase (2-5A synthetase). We show that mouse L cells expressing nonsecreted (intracellular) type I human IFN are less susceptible to encephalomyocarditis (EMC) virus infection and have increased levels of 2-5A synthetase. The 2-5A synthetase promoter is constitutively induced, and the antiviral effects are most likely mediated through activation of ISGF3, which occurs constitutively in cell lines expressing intracellular interferon. These data suggest that the internalization of IFN-α may play a role in the antiviral properties associated with IFN.

Original languageEnglish
Pages (from-to)507-510
Number of pages4
JournalJournal of Interferon and Cytokine Research
Issue number7
Publication statusPublished - Jul 1996
Externally publishedYes

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