Innate immune pattern-recognition receptors sensing influenza viral RNA (PRRs)

Innate immune pattern-recognition receptors (PRRs) that sense influenza viral RNA represent a critical class of sensors responsible for detecting the presence of viral genetic material during infection. This group primarily includes Retinoic acid-inducible gene I (RIG-I), which detects 5'-triphosphorylated or diphosphorylated short double-stranded RNA in the cytoplasm, and Toll-like receptors (TLR7 and TLR3), which sense single-stranded and double-stranded RNA within endosomes. Upon activation, these receptors initiate signaling cascades involving adaptor proteins like MAVS or MyD88, leading to the activation of transcription factors such as IRF3/7 and NF-κB. This process results in the robust production of Type I interferons and pro-inflammatory cytokines, which are essential for limiting viral replication and orchestrating the adaptive immune response. While these receptors are vital for host defense against influenza, their overactivation can contribute to severe immunopathology, such as the 'cytokine storm' observed in highly pathogenic avian influenza infections. Consequently, they are being explored as therapeutic targets for both antiviral adjuvants and immunomodulatory treatments.

Other names

Pattern recognition receptorsRNA-sensing PRRsInfluenza virus sensorsRIG-I-like receptorsToll-like receptorsNOD-like receptors

Agonists of these receptors (e.g., TLR7/8 or RIG-I ligands) mimic viral RNA to trigger the production of Type I interferons and pro-inflammatory cytokines, thereby enhancing the innate and adaptive immune response against viral infections or tumors.