This targeted presentation of IFN-β at the viral surface is qualitatively different from subcutaneous or intravenous IFN-β administration, which leads to systemic distribution of IFN-β coupled with highly diffuse antiviral action, low IFN-β concentrations at the site of infection, and a primary impact on non-target cell types irrelevant to the viral infection. This evidence concerns the gene IFNB1 and infection.