Innate antiviral pathways

Innate antiviral pathways constitute the primary defense mechanism of the host against viral pathogens, relying on the recognition of conserved viral components known as pathogen-associated molecular patterns (PAMPs). These pathways are initiated by various pattern recognition receptors (PRRs), including Toll-like receptors (TLRs), RIG-I-like receptors (RLRs), and the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway (Chen et al., 2016, Nat Immunol). Activation of these sensors triggers complex signaling cascades involving adaptor proteins like MyD88, TRIF, MAVS, and STING, ultimately leading to the activation of transcription factors such as IRF3, IRF7, and NF-kB (Akira et al., 2006, Nat Rev Immunol). This results in the robust production of type I and III interferons (IFNs) and pro-inflammatory cytokines, which establish an antiviral state in both infected and neighboring cells by inducing hundreds of interferon-stimulated genes (ISGs) (Schneider et al., 2014, Annu Rev Immunol). Beyond infection, these pathways play critical roles in cancer immunosurveillance and the pathogenesis of autoimmune diseases like systemic lupus erythematosus (Loo & Gale, 2011, Immunity). Pharmacological modulation of these pathways, such as through TLR or STING agonists, is a major area of research for developing novel antivirals and cancer immunotherapies, while inhibitors are sought for treating autoinflammatory conditions.

Other names

Innate immune response to virusesAntiviral innate immunityPattern recognition receptor signalingType I interferon signaling pathways

Activation of pattern recognition receptors (PRRs) such as TLRs, RLRs, and cGAS-STING to induce the expression of type I interferons and interferon-stimulated genes (ISGs).