These loci/mutations were chosen to increase IFN sensitivity (5’U4&6) [28]; decrease HS binding and neurovirulence and increase virus particle access to lymphoid tissue (E71-77) [33]; decrease shutoff of host cell transcription, thereby, increasing host cell responses to infection and potentially antigen presentation in infected cells (C65-59) [32]; and eliminate miR-142-3p restriction, thus increasing myeloid cell replication, direct antigen presentation and cytokine responses (3’U11337) [35]. The gene discussed is IFNA1; the disease is infection.