Overall, these findings suggest that B. coccoides is sufficient for maintaining optimal mononuclear phagocyte responsiveness to stimuli (cytokine and viral infection), and it seems very likely that B. coccoides augments type I IFN signaling in mononuclear phagocytes via IFNAR and STAT1 phosphorylation to protect the host from virus systemic infection. Here, IFNAR1 is linked to viral infectious disease.