Most mammalian species have multiple IFN-a subtypes. Although the reasons for these multiple subtypes are not fully known, there are clear cell type and temporal differences in their expression. A recent study established a nomenclature for the murine IFN-a subtypes (van Pesch et al. 2004) and determined relative activities of the subtypes with protein quantification by phosphorimaging of metabolically-labeled protein. In this study, Mu IFN-a4 was deemed to have average antiviral activity when compared with the potency of the other subtypes. Mu IFN-a4 was initially cloned by Zwarthoff et al. [(1985) Nuc. Acids Res. 13(3) 791], and has been extensively studied. It is apparently expressed early in viral infection in a protein synthesis independent manner, and its expression is induced by phosphorylation of IRF-3. It may be that Mu IFN-a4, like IFN-b, has a priming function on cells, enabling the expression of other Mu IFN-a subtypes [Reviewed by Mesplède et al. (2003) Autoimmunity 36(8):447 and Asselin-Paturel & Trinchieri (2005) J. Exp. Med. 202(4):461]. Thus, this interferon is among the first observed after viral infection. Intriguingly, while this interferon is expressed in a large variety of cell types, one report suggests that the expression level in dendritic cells is low to non-existent [Barchet et al. (2002) J. Exp. Med. 195(4):507]