Inflammatory and Viral Replication Signaling Pathways

"Inflammatory and viral replication signaling pathways" describe interconnected cellular signaling networks—such as the Toll-like receptor (TLR), Interferon (IFN), Janus kinase-signal transducers and activators of transcription (JAK-STAT), mitogen-activated protein kinase (MAPK), nuclear factor kappa B (NF-κB), and stimulator of interferon genes (STING) pathways—that sense viral infection, coordinate immune responses, induce inflammatory mediators, and regulate apoptosis and antiviral defense. Dysregulation of these pathways can result in severe immunopathology (such as cytokine storm in COVID-19 and sepsis), while viral pathogens often evolve mechanisms to evade, suppress, or hijack these responses to favor their replication. Because these signaling cascades are crucial for determining infection outcomes, many of their constituent molecular components are individually considered drug targets in immunology and infectious disease—it is therefore important to specify the particular molecule to discuss true drug targeting or therapeutic intervention.

Other names

Inflammatory signaling pathwaysViral replication signaling pathwaysHost antiviral signaling pathwaysImmunoinflammatory signaling networks

Inhibition of cytokine production (e.g., blocking IL-6, TNF-α pathways); Suppression of kinase activity (JAK inhibitors, MAPK inhibitors); Inhibition of transcription factor activation (e.g., NF-κB inhibitors); Downregulation of inflammatory gene expression