tetano
Editor, Senior Moderator
Nat Commun
. 2025 Feb 17;16(1):1715.
doi: 10.1038/s41467-025-57094-0. The CXCL8/MAPK/hnRNP-K axis enables susceptibility to infection by EV-D68, rhinovirus, and influenza virus in vitro
Qingran Yang[SUP] 1 2 [/SUP], Haoran Guo[SUP] 2 [/SUP], Huili Li[SUP] 2 [/SUP], Zhaoxue Li[SUP] 2 [/SUP], Fushun Ni[SUP] 2 [/SUP], Zhongmei Wen[SUP] 3 [/SUP], Kai Liu[SUP] 4 [/SUP], Huihui Kong[SUP] 5 6 [/SUP], Wei Wei[SUP] 7 8 [/SUP]
Affiliations
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.
. 2025 Feb 17;16(1):1715.
doi: 10.1038/s41467-025-57094-0. The CXCL8/MAPK/hnRNP-K axis enables susceptibility to infection by EV-D68, rhinovirus, and influenza virus in vitro
Qingran Yang[SUP] 1 2 [/SUP], Haoran Guo[SUP] 2 [/SUP], Huili Li[SUP] 2 [/SUP], Zhaoxue Li[SUP] 2 [/SUP], Fushun Ni[SUP] 2 [/SUP], Zhongmei Wen[SUP] 3 [/SUP], Kai Liu[SUP] 4 [/SUP], Huihui Kong[SUP] 5 6 [/SUP], Wei Wei[SUP] 7 8 [/SUP]
Affiliations
- PMID: 39962077
- DOI: 10.1038/s41467-025-57094-0
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.