[No authors listed]
Two serologically distinct type I interferons (IFNs), designated ChIFN1 and ChIFN2, are known in the chicken. ChIFN1 is encoded by a family of 10 or more genes, whereas ChIFN2 is encoded by a single gene. We show here that ChIFN1 and ChIFN2 transcripts are both strongly induced by Newcastle disease virus in primary chicken macrophages. By contrast, oral administration of the imidazoquinoline S-28463, which selectively induces IFN-alpha in mammals, led to a rapid accumulation of ChIFN1 (but not ChIFN2) transcripts in adult chicken spleen and thymus. The 5'-upstream region of the ChIFN2 gene contains a NF-kappaB consensus motif flanked by a sequence element that could serve as a binding site for transcription factor IRF-1, reminiscent of mammalian IFN-beta promoters, and it mediated powerful virus inducibility in a duck fibroblast cell line when cloned in front of a promoterless luciferase reporter gene. The 5'-upstream region of the cloned ChIFN1 gene contains two putative binding sites for IRF-1, but lacks NF-kappaB-binding sites, and it did not respond well to virus in transfected cells. Thus, the promoters of ChIFN1 and ChIFN2 genes not only exhibited differential responses to nonviral inducers in vivo, but also differed in structure and response to virus in transfected cells. These findings indicate that ChIFN2 represents the avian homolog of mammalian IFN-beta, whereas ChIFN1 seems to correspond to mammalian IFN-alpha.
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