Host antiviral immune response pathways

Host antiviral immune response pathways are the collective biological processes and signaling cascades employed by a host organism to detect, contain, and eliminate viral pathogens (Nature Reviews Immunology, 2020). These pathways are initiated by pattern recognition receptors (PRRs) such as Toll-like receptors (TLRs), RIG-I-like receptors (RLRs), and the cGAS-STING pathway, which sense viral nucleic acids and proteins (Frontiers in Immunology, 2021). Upon activation, these receptors trigger signaling through adapter proteins like MAVS and STING, leading to the activation of transcription factors such as IRF3, IRF7, and NF-kB (NIH, 2022). This results in the production of type I and III interferons and pro-inflammatory cytokines, which induce an 'antiviral state' in neighboring cells by upregulating hundreds of interferon-stimulated genes (ISGs) that inhibit viral replication (PubMed, 2019). While essential for defense, excessive or chronic activation of these pathways can lead to severe inflammation, tissue damage, and autoimmune diseases (StatPearls, 2023). Therapeutic strategies include agonists to enhance the response against chronic viral infections or cancer, and inhibitors like JAK inhibitors or interferon-blocking antibodies to manage hyper-inflammatory states (Nature, 2021).

Other names

Antiviral innate immunityHost defense pathwaysInterferon response pathwaysInnate immune sensing pathwaysAntiviral signaling pathways

Modulation of innate immune sensing (e.g., TLR/RLR agonists), interferon signaling (e.g., IFN-alpha), or downstream effector production to inhibit viral replication; or inhibition of these pathways (e.g., JAK inhibitors or interferon-blocking antibodies) to prevent hyper-inflammation.