2. Academic Validation
  3. The CXCL8/MAPK/hnRNP-K axis enables susceptibility to infection by EV-D68, rhinovirus, and influenza virus in vitro

The CXCL8/MAPK/hnRNP-K axis enables susceptibility to infection by EV-D68, rhinovirus, and influenza virus in vitro

  • Nat Commun. 2025 Feb 17;16(1):1715. doi: 10.1038/s41467-025-57094-0.
Qingran Yang 1 2,  Haoran Guo 2,  Huili Li 2,  Zhaoxue Li 2,  Fushun Ni 2,  Zhongmei Wen 3,  Kai Liu 4,  Huihui Kong 5 6,  Wei Wei 7 8
Affiliations

Affiliations

  • 1 Department of Respiration, Children's Medical Center, First Hospital, Jilin University, Changchun, Jilin, China.
  • 2 Institute of Virology and AIDS Research, First Hospital, Jilin University, Changchun, Jilin, China.
  • 3 Center for Pathogen Biology and Infectious Diseases, Department of Respiratory Medicine, First Hospital, Jilin University, Changchun, Jilin, China.
  • 4 Department of Chemistry, Tsinghua University, Beijing, China.
  • 5 Influenza Research Institute, Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, Madison, WI, USA.
  • 6 State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, the Chinese Academy of Agricultural Sciences, Harbin, China.
  • 7 Institute of Virology and AIDS Research, First Hospital, Jilin University, Changchun, Jilin, China. wwei6@jlu.edu.cn.
  • 8 Cancer Center, Key Laboratory of Organ Regeneration and Transplantation of Ministry of Education, Institute of Translational Medicine, First Hospital, Jilin University, Changchun, Jilin, China. wwei6@jlu.edu.cn.
PMID: 39962077 DOI: 10.1038/s41467-025-57094-0
Abstract

Respiratory viruses pose an ongoing threat to human health with excessive cytokine secretion contributing to severe illness and mortality. However, the relationship between cytokine secretion and viral Infection remains poorly understood. Here we elucidate the role of CXCL8 as an early response gene to EV-D68 Infection. Silencing CXCL8 or its receptors, CXCR1/2, impedes EV-D68 replication in vitro. Upon recognition of CXCL8 by CXCR1/2, the MAPK pathway is activated, facilitating the translocation of nuclear hnRNP-K to the cytoplasm. This translocation increases the recognition of viral RNA by hnRNP-K in the cytoplasm, promoting the function of the 5' untranslated region in the viral genome. Moreover, our investigations also reveal the importance of the CXCL8 signaling pathway in the replication of both Influenza Virus and rhinovirus. In summary, our findings hint that these viruses exploit the CXCL8/MAPK/hnRNP-K axis to enhance viral replication in respiratory cells in vitro.

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