Consistent with this, no decrease in iregDC, PDL1, IL-10 or increase in stimDC occurred in LCMV-Cl13 infected IFNβ-/- mice (S3C Fig), indicating that IFNβ alone does not drive immunosuppression or iregDC differentiation during viral persistence and suggests in part why IFNβ antibody blockade may not be as efficient for controlling infection as blocking all IFNαR signaling. The gene discussed is IFNB1; the disease is infection.