The IFN-β enhanceosome, a protein complex activated by viral infection, regulates IFN-β gene expression crucial for innate antiviral immune response. Formed by transcription factors like IRF3, NF-κB, ATF-2/c-Jun, and coactivators like CBP/p300, it binds to IFN-β promoter, activating gene expression and inducing the immune response.

Upon recognizing viral RNA, RIG-I-like receptors (RLRs) undergo conformational changes, interacting with MAVS to activate TRAFs. This leads to downstream signaling pathways, including IRF3 activation for interferon gene transcription, NF-κB activation for pro-inflammatory cytokine regulation, and MAPK pathway activation through AP-1, orchestrating a robust antiviral immune response.

In contrast to endotoxin tolerance, innate immune response can be heightened and "trained" after primary exposure to pathogen-associated molecular patterns (PAMPs), particularly through C-type lectin receptors (CLRs). This results in enhanced immune cell responsiveness, epigenetic reprogramming, metabolic changes, increased cytokine production, antimicrobial activity, and memory-like characteristics. Innate immune training provides broad protection, influences vaccination strategies, and has implications for pathological conditions.