Reverse-regulation of hemichannel/gap junction channels in virus-induced innate and adaptive immune responses

Cell–cell communication plays a pivotal role in shaping innate and adaptive immune responses during viral infection. Recent studies show that viral replication and immune signaling are closely linked to the regulation of hemichannels and gap junction channels formed by Innexin, Connexin, and Pannexin proteins. Viruses often exploit these channels to facilitate spread, suppress antiviral signaling, or modulate host metabolism. Conversely, a “reverse-regulation” mechanism — involving controlled channel opening or closure — has emerged as a host strategy to counteract viral evasion. By restoring metabolic and immunological equilibrium, reverse-regulation restricts viral replication and mitigates cell injury, highlighting a key yet underexplored stress-response mechanism linking intercellular or extracellular communication with viral immunity. Despite advances in single-cell sequencing and molecular virology, the exact signaling networks and cross-species conservation of these processes remain largely undefined.This Research Topic aims to elucidate how reverse-regulation of hemichannel and gap junction channel dynamics contributes to antiviral defense and immune homeostasis across different biological systems. It seeks to clarify how viruses modulate channel behavior to interfere with immune signaling and how host cells adapt their communication networks to restore antiviral competence. By integrating knowledge from diverse organisms — including plants, invertebrates, vertebrates, and microbes — this topic encourages comparative and mechanistic approaches. Special emphasis is placed on identifying molecular determinants that govern the bidirectional regulation of Innexin, Connexin, and Pannexin proteins and their implications for immune modulation, stress adaptation, and viral pathogenesis. To gather further insights into the cross-species regulation of cell–cell communication during viral infection, we welcome contributions that explore experimental, computational, and translational perspectives on hemichannel/gap junction channel regulation. We invite submissions of original research, reviews, and methods papers addressing, but not limited to, the following themes:• Virus–Innexin interactions in innate immune responses• Virus–Connexin/Pannexin modulation in innate and adaptive immunity• Single-cell sequencing of Innexin expression and regulation in invertebrate antiviral defense• Single-cell sequencing and functional characterization of Connexin/Pannexin isoforms in vertebrate immunity• Comparative analyses of virus–immunity communication networks across species• Alternative mechanisms linking gap junction signaling with antiviral responses Topic editors: Yongliang Zhang, Kai-Jun Luo, Zigui Chen Source: https://www.frontiersin.org/research-topics/82395/reverse-regulation-of-hemichannelgap-junction-channels-in-virus-induced-innate-and-adaptive-immune-responses