Antiviral Activity of Autocrine Interferon-β Requires the Presence of a Functional Interferon Type I Receptor

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Abstract
We and others have previously observed that the antiviral effects of autocrine interferon (IFN)-α/β activity cannot be abolished by neutralizing antibodies, even when present to a large excess. This raises the possibility that the major part of autocrine activity is triggered intracellularly, possibly bypassing the transmembrane IFN-α/β receptor. To examine this possibility, cells derived from IFN-α/βRo/o knockout mice lacking a functional IFN-α/β receptor were stably transformed with pHMB-KbMuIFNβ or pMFG-MuIFNβ plasmids encoding a constitutively expressed murine IFN-β gene. Four different clones were isolated and examined for resistance to a retrovirus, MFG-LacZ, and to Semliki Forest virus. Despite the production of autocrine IFN-β at levels inducing high antiviral resistance in control cells, none of the clones displayed antiviral resistance. Thus, despite its failure to be neutralized by potent antiserum, the antiviral activity of autocrine IFN-β takes place via the transmembrane IFN-α/β receptor, and no additional pathway is involved.