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Intracellular antiviral defense pathways are a collection of innate immune mechanisms that detect and respond to viral invasion within host cells (Nature Reviews Immunology, 2020). These pathways utilize pattern recognition receptors (PRRs) such as RIG-I-like receptors (RLRs), Toll-like receptors (TLRs), and the cGAS-STING pathway to identify viral pathogen-associated molecular patterns (PAMPs), primarily viral nucleic acids (Cell, 2016). Activation of these sensors triggers signaling cascades involving adaptor proteins like MAVS, TRIF, or STING, which activate transcription factors such as IRF3, IRF7, and NF-κB (Annual Review of Immunology, 2019). This leads to the synthesis and secretion of Type I and Type III interferons (IFNs), which act in autocrine and paracrine manners to induce an antiviral state by upregulating hundreds of interferon-stimulated genes (ISGs) (Science, 2015). These ISGs, including OAS1 and PKR, directly inhibit viral replication, protein synthesis, and assembly (Journal of Virology, 2017). While critical for host defense against viruses like Influenza and SARS-CoV-2, chronic activation of these pathways is linked to interferonopathies and autoimmune diseases (Nature, 2014). Pharmacological modulation includes the use of IFN analogs and PRR agonists for viral infections and oncology, as well as inhibitors for inflammatory conditions (Drug Discovery Today, 2021).
Activation or modulation of pattern recognition receptors and downstream signaling to induce interferon production and an antiviral state.
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