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Extracellular nucleoprotein exacerbates influenza viruspathogenesis by activating Toll-like receptor 4 and the NLRP3inflammasome

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Cellular & Molecular Immunology 2022年第6期19卷 715-725页

作者： Chang-Ung Kim Yu-Jin Jeong pureum lee Moo-Seung lee Jong-Hwan Park Young-Sang Kim Doo-Jin Kim Infectious Disease Research Center Korea Research Institute of Bioscience and Biotechnology(KRIBB)DaejeonSouth Korea Department of Biochemistry Chungnam National UniversityDaejeonSouth Korea Environmental Diseases Research Center Korea Research Institute of Bioscience and Biotechnology(KRIBB)DaejeonSouth Korea University of Science and Technology(UST) DaejeonSouth Korea College of Veterinary Medicine Chonnam National UniversityGwangjuSouth Korea

Host immune responses, such as those initiated by pattern recognition receptor (PRR) activation, are important for viralclearance and pathogenesis. However, little is known about the interactions of viral proteins with surface PRRs or, moreimportantly, the association of innate immune activation with viral pathogenesis. In this study, we showed that internalinfluenza virus proteins were released from infected cells. Among these proteins, nucleoprotein (NP) played a critical role inviral pathogenesis by stimulating neighboring cells through toll-like receptor (TLR)2, TLR4, and the NLR family pyrin domaincontaining 3 (NLRP3) inflammasome. Through the activation of these PRRs, NP induced the production of interleukin (IL)-1β andIL-6, which subsequently led to the induction of trypsin. Trypsin induced by NP increased the infectivity of influenza virus,leading to increases in viral replication and pathology upon subsequent viral infection. These results reveal the role of releasedNP in influenza pathogenesis and highlight the importance of the interactions of internal viral proteins with PRRs in theextracellular compartment during viral pathogenesis.

关键词： Influenza virus Viral protein release Nucleoprotein Toll-like receptor Cyotkine-trypsin cycle

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