The innate immune system relies on innate immune sensors, such as pattern recognition receptors (PRRs), to detect pathogens and initiate immune responses, crucial for controlling infections but also implicated in inflammatory diseases. These innate immune sensors, including Toll-like receptors (TLRs), nod-like receptors (NLRs), RIG-I-like receptors (RLRs), absent in melanoma 2 (AIM2), and Z-DNA binding protein 1 (ZBP1) trigger signaling pathways that produce cytokines, modulating inflammation and cell death. Traditional therapies focus on directly targeting pathogens; however, host-targeting therapeutic strategies have emerged as innovative approaches to modulate innate immune sensor activity. These strategies aim to fine-tune the immune response, either enhancing antiviral defenses or mitigating hyperinflammation to prevent tissue damage. This review explores innate immune sensor-based therapeutic approaches, including inhibitors, agonists, and antagonists, that enhance antiviral defense or suppress harmful inflammation, highlighting innate immune sensors as promising targets in infectious and inflammatory disease treatment.

Korean Red ginseng has emerged as a potent candidate in the fight against various viral infections, demonstrating significant efficacy both in vitro and in vivo, particularly against influenza A viruses. Despite substantial evidence of its antiviral properties, the detailed molecular mechanisms through which it reduces viral lethality remain insufficiently understood. Our investigations have highlighted the superior effectiveness of Korean Red ginseng against influenza viruses, outperforming its effects on numerous other viral strains. We aim to uncover the specific mechanisms by which Korean Red ginseng exerts its antiviral effects, focusing on influenza A viruses. Our prior studies have identified the role of Z-DNA-binding protein 1 (ZBP1), a signaling complex involved in inducing programmed cell death in response to influenza virus infection. Given the critical role of ZBP1 as a sensor for viral nucleic acid, we hypothesize that Korean Red ginseng may modulate the ZBP1-derived cell death pathway. This interaction is anticipated to enhance cell death while concurrently suppressing viral protein expression, offering novel insights into the antiviral mechanism of Korean Red ginseng against influenza A viruses.