MX1 and viral infectious disease: We hypothesize that this phenomenon may be attributed to the activation of innate immune signaling pathways by viral infection, which in turn activates the IFN-β promoter and upregulates antiviral molecules (such as OAS, PKR, and MxA) as well as inflammatory cytokines (including IL-2, IL-6, IFN-α, and IFN-γ).