MYD88 and Immunodeficiency: Hence, to generalize our observation that very low levels of IFN-I production are sufficient to induce strong IFN-I responses, we next measured pangenomic ISG induction in mice with low serum IFN-I titers (Fig 1C) and splenic pDC IFN-I expression (S2A and S2D Fig) resulting either from a primary immune deficiency (MyD88-/- animals) or on the contrary from early control of the virus by NK cells (Ly49H+ animals).