Evidence map›Paper›PMID 42505341›Full record

ArticleJournal of virology2026

c-Fos enhances influenza virus replication by stabilizing the M2 protein and promoting autophagosome accumulation.

Xiaonan Chen, Junyang Yan, Mengxue Li, Hanbin Liu, Daiqiang Lu, Yang Wang, Yun Liu, Qiao Zhang, Feng Gao, Jiaojiao Peng

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of virology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
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0citing papers in PubMed
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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

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3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

10 authors.

Xiaonan ChenInstitute of Molecular and Medical Virology, School of Medicine, Jinan University, Guangzhou, China.
Junyang YanInstitute of Molecular and Medical Virology, School of Medicine, Jinan University, Guangzhou, China.
Mengxue LiInstitute of Molecular and Medical Virology, School of Medicine, Jinan University, Guangzhou, China.
Hanbin LiuGuangdong Zocode Biotechnology Services Co., Ltd, Guangzhou, China.
Daiqiang LuInstitute of Molecular and Medical Virology, School of Medicine, Jinan University, Guangzhou, China.
Yang WangState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, National Center for Respiratory Medicine, Guangzhou Institute of Respiratory Health, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.ORCID 0000-0002-6527-864X
Yun LiuSchool of Stomatology, Jinan University, Guangzhou, China.
Qiao ZhangInstitute of Molecular and Medical Virology, School of Medicine, Jinan University, Guangzhou, China.
Feng GaoInstitute of Molecular and Medical Virology, School of Medicine, Jinan University, Guangzhou, China.ORCID 0000-0001-8903-0203
Jiaojiao PengInstitute of Molecular and Medical Virology, School of Medicine, Jinan University, Guangzhou, China.ORCID 0009-0002-7042-4450

Funding

Guangdong Basic and Applied Basic Research Foundation 2025A1515012487Guangdong Basic and Applied Basic Research Foundation 2025A1515012645The Innovation and Entrepreneurship Training Program for Undergraduate of Guangdong Province S202510559159The Open Research Project of the Key Laboratory of Viral Pathogenesis & Infection Prevention and Control of the Ministry of Education 2023VPPC-R04The Pearl River Innovation and Entrepreneurship Team 2021ZT09Y552
6 · The paper itself

Abstract

The influenza A virus (IAV) employs multiple strategies to hijack host cellular machinery for efficient replication. While autophagosome accumulation is known to promote IAV replication, and the viral matrix protein 2 (M2) ion channel protein plays essential roles in viral uncoating, assembly, and autophagosome accumulation, the mechanisms regulating M2 stability remain incompletely understood. Our previous work established that IAV inhibits SERCA activity to trigger autophagosome accumulation. Here, we identify c-Fos as a critical downstream mediator that stabilizes M2, thereby promoting both autophagosome accumulation and viral replication. Mechanistically, IAV infection drives M2-dependent cytosolic calcium elevation, which upregulates c-Fos expression. The induced c-Fos then binds to M2, protecting it from proteasomal and lysosomal degradation and thereby increasing M2 abundance. This stabilized M2 not only directly enhances viral replication but also sustains autophagosome accumulation to further augment viral growth. Collectively, our findings establish c-Fos as a key regulator of IAV replication via M2 stabilization, revealing a novel mechanism by which the virus amplifies its propagation. These interactions represent potential therapeutic targets for antiviral intervention.

Indexed as

AutophagosomesInfluenza A virusProto-Oncogene Proteins c-fosViral Matrix ProteinsVirus ReplicationA549 CellsAnimalsCalciumDogsHost-Pathogen InteractionsHumansInfluenza, HumanMadin Darby Canine Kidney CellsProtein StabilityViroporin ProteinsCalciumFOS protein, humanM2 protein, Influenza A virusProto-Oncogene Proteins c-fosViral Matrix ProteinsViroporin Proteinsautophagyc-Fosinfluenza virusM2 proteinviral replication

Identifiers

PMID42505341
PMCPMC13483408

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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.