Evidence map›Paper›PMID 39962077›Full record

ArticleNature communications2025

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

Qingran Yang, Haoran Guo, Huili Li, Zhaoxue Li, Fushun Ni, Zhongmei Wen, Kai Liu, Huihui Kong, Wei Wei

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed.

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  11. Mechanisms of host-bacterial interactions duringFrontiers in veterinary science · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Qingran YangDepartment of Respiration, Children's Medical Center, First Hospital, Jilin University, Changchun, Jilin, China.ORCID http://orcid.org/0009-0005-3007-1808
Haoran GuoInstitute of Virology and AIDS Research, First Hospital, Jilin University, Changchun, Jilin, China.
Huili LiInstitute of Virology and AIDS Research, First Hospital, Jilin University, Changchun, Jilin, China.
Zhaoxue LiInstitute of Virology and AIDS Research, First Hospital, Jilin University, Changchun, Jilin, China.
Fushun NiInstitute of Virology and AIDS Research, First Hospital, Jilin University, Changchun, Jilin, China.
Zhongmei WenCenter for Pathogen Biology and Infectious Diseases, Department of Respiratory Medicine, First Hospital, Jilin University, Changchun, Jilin, China.
Kai LiuDepartment of Chemistry, Tsinghua University, Beijing, China.ORCID http://orcid.org/0000-0003-0878-5191
Huihui KongInfluenza Research Institute, Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, Madison, WI, USA.
Wei WeiInstitute of Virology and AIDS Research, First Hospital, Jilin University, Changchun, Jilin, China. wwei6@jlu.edu.cn.ORCID http://orcid.org/0000-0003-4456-840X

Funding

National Natural Science Foundation of China (National Science Foundation of China) 32222005National Natural Science Foundation of China (National Science Foundation of China) 82372226
6 · The paper itself

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.

Indexed as

Influenza, HumanInterleukin-8OrthomyxoviridaeRhinovirusA549 CellsAnimalsHumansMAP Kinase Signaling SystemRNA, ViralSignal TransductionVirus ReplicationCXCL8 protein, humanInterleukin-8RNA, Viral

Identifiers

PMID39962077
PMCPMC11832783

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.