In PRV, we reported that the increased IFNalpha production by PBMCs/pDCs in response to gEnull PRV-infected cells compared with WT PRV-infected cells correlates with an increased production of pDC-activating extracellular virus particles at relatively early time points post infection with gEnull PRV compared with WT PRV [16]. The gene discussed is IFNA1; the disease is infection.