Host antiviral immune pathways

Host antiviral immune pathways represent the collective innate and adaptive defense mechanisms employed by a host organism to detect, restrict, and eliminate viral infections (1.1.4, 1.3.4). These pathways are triggered by the recognition of pathogen-associated molecular patterns (PAMPs) by various host sensors, including Toll-like receptors (TLRs), RIG-I-like receptors (RLRs), and the cGAS-STING pathway (1.2.3, 1.3.4). Upon activation, these sensors initiate signaling cascades that culminate in the production of type I and III interferons (IFNs) and other pro-inflammatory cytokines (1.1.4). These molecules then signal through their respective receptors to induce the expression of interferon-stimulated genes (ISGs), which exert direct antiviral effects by inhibiting viral entry, replication, and assembly (1.3.4). In many viral diseases, such as COVID-19 or chronic hepatitis, the virus may evade these pathways or the host response may become pathologically overactive, leading to tissue damage (1.2.3, 1.3.3). Therapeutic intervention involves either stimulating these pathways with agonists (e.g., TLR or STING agonists) and exogenous IFNs to enhance viral clearance or using inhibitors (e.g., JAK inhibitors) to mitigate excessive inflammation (1.2.1, 1.3.2). Host-directed therapies targeting these pathways offer a broad-spectrum approach that is less prone to viral resistance compared to direct-acting antivirals (1.2.1, 1.2.2). However, modulating these pathways requires careful management to avoid systemic toxicity or autoimmune reactions (1.2.1).

Other names

Host innate immune pathwaysAntiviral innate immunityHost-directed antiviral pathwaysInnate immune signaling pathways

Activation of innate immune sensors (TLRs, RLRs, cGAS-STING), induction of type I/III interferon signaling, and stimulation of interferon-stimulated gene (ISG) expression to inhibit viral replication.