Triggering of PRRs induces the production of host proinflammatory cytokines (e.g. TNF, IL-6 and IL-1) and type I interferons (interferon-α (IFN-α) and IFN-β) through activation of downstream signaling pathways that control various transcription factors such as NF-κB, AP-1, IRF3 and IRF7 [1], [2].