Innate Immune Sensing and Evasion Mechanisms in Viral Infections: From Fundamental Biology to Clinical Translation

Dear Colleagues,

Innate immune responses constitute the earliest defense mechanism against viral invasion and critically influence infection outcomes and disease severity. Host cells utilize diverse pattern recognition receptors (PRRs), including Toll-like receptors (TLRs), RIG-I-like receptors (RLRs), NOD-like receptors (NLRs), and cytosolic nucleic acid sensors, to detect pathogen-associated and danger-associated molecular signals. Activation of these pathways stimulates the production of type I interferons, inflammatory mediators, and antiviral effector molecules that coordinate protective immunity.

Despite these defense mechanisms, viruses have evolved multiple strategies to disrupt host innate immune signaling, thereby promoting replication, persistence, and disease progression. In addition, excessive or dysregulated innate immune activation may contribute to tissue injury, chronic inflammation, and severe clinical manifestations. Therefore, deeper insight into host sensing pathways and viral countermeasures is essential for advancing antiviral therapies, vaccine design, and immune-targeted interventions.

This Special Issue welcomes original research articles, reviews, and perspectives focusing on the molecular mechanisms and translational implications of innate immune sensing and viral immune evasion.

Topics of interest include, but are not limited to, the following:

• Innate immune sensing pathways during viral infections;
• Viral strategies for immune evasion and immune modulation;
• PRR-mediated antiviral signaling and host defense;
• Cytokine and interferon responses in viral pathogenesis;
• Innate immunity-based antiviral therapeutics and vaccines;
• Translational and clinical applications targeting innate immune pathways.

Dr. Mohammad Enamul Hoque Kayesh
Guest Editor

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