Evidence map›Paper›PMID 42017991›Full record

ArticleCellular and molecular life sciences : CMLS2026

LC3-associated phagocytosis is a new strategy to inhibit picornavirus infection through increasing interferon levels and lysosomal degradation.

Xiuping Wu, Yi Ru, Wei Zhang, Rongzeng Hao, Xiaodong Qin, Haimi Dang, Dongmei Zhao, Bingzhou Lu, Yajun Li, Shengzhen Sun and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 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
0cells of the map it votes in
0citing 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

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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

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

12 authors.

Xiuping Wu *State Key Laboratory of Animal Disease Control and Prevention, College of Veterinary Medicine, Lanzhou University, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, 730000, China.
Yi Ru *State Key Laboratory of Animal Disease Control and Prevention, College of Veterinary Medicine, Lanzhou University, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, 730000, China.
Wei Zhang *State Key Laboratory of Animal Disease Control and Prevention, College of Veterinary Medicine, Lanzhou University, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, 730000, China.
Rongzeng HaoState Key Laboratory of Animal Disease Control and Prevention, College of Veterinary Medicine, Lanzhou University, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, 730000, China.
Xiaodong QinState Key Laboratory of Animal Disease Control and Prevention, College of Veterinary Medicine, Lanzhou University, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, 730000, China.
Haimi DangState Key Laboratory of Animal Disease Control and Prevention, College of Veterinary Medicine, Lanzhou University, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, 730000, China.
Dongmei ZhaoState Key Laboratory of Animal Disease Control and Prevention, College of Veterinary Medicine, Lanzhou University, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, 730000, China.
Bingzhou LuState Key Laboratory of Animal Disease Control and Prevention, College of Veterinary Medicine, Lanzhou University, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, 730000, China.
Yajun LiState Key Laboratory of Animal Disease Control and Prevention, College of Veterinary Medicine, Lanzhou University, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, 730000, China.
Shengzhen SunState Key Laboratory of Animal Disease Control and Prevention, College of Veterinary Medicine, Lanzhou University, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, 730000, China.
Yang YangState Key Laboratory of Animal Disease Control and Prevention, College of Veterinary Medicine, Lanzhou University, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, 730000, China. yangyang01@caas.cn.
Haixue ZhengState Key Laboratory of Animal Disease Control and Prevention, College of Veterinary Medicine, Lanzhou University, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, 730000, China. zhenghaixue@caas.cn.ORCID http://orcid.org/0009-0007-2638-3934

Funding

Innovative Research Group Project of the National Natural Science Foundation of China 32372990Major Basic Research Project of the Natural Science Foundation of the Jiangsu Higher Education Institutions 23YFNA0011the Natural Scienc the Natural Sciences Foundation of Gansu Province es Foundation of Gansu Province 23JRRA549
6 · The paper itself

Abstract

LC3-associated phagocytosis (LAP) is a novel type of noncanonical autophagy that contributes to inflammatory responses and immune regulation in various cell and tissue types infected by DNA and RNA viruses. The role of LAP during picornavirus infection remains unclear. Here, using PK-15 cells, Vero cells and mice lacking the WD domain of ATG16L1 as a LAP deficient model, we found that infection with foot-and-mouth disease virus (FMDV), senecavirus A (SVA), and enterovirus 71 (EV71) induced LAP, and LAP inhibited the replication of these viruses. Further investigation revealed that LAP inhibited FMDV replication through increasing interferon levels and promoting lysosomal degradation. In addition, GBP1, IFITM3, OASL, IIFIT1, Mx1 and other innate immune factors related to the interferon pathway were significantly inhibited in LAP-deficient cells during FMDV infection. Furthermore, LAP-deficient mice were more susceptible to FMDV, with greater lethality and more severe pathological damage and viral loads in the blood, heart, spleen, liver, lungs and kidneys. In conclusion, this study uncovers a novel mechanism of the host antiviral effect of LAP on picornaviruses and provides a theoretical basis for the development of new antiviral strategies against picornaviruses.Importance:FMDV, SVA and EV71 all belong to the Picornaviridae family, which has single-stranded positive-sense RNA, is nonenveloped and can cause diseases in both humans and animals. A noncanonical function of the autophagy machinery known as LC3-associated phagocytosis (LAP), utilizes a portion of components of the canonical autophagy machinery, is one of the important ways for cells to cope with pathogen infection. This study revealed a new strategy to inhibit picornavirus replication through increasing interferon levels and promoting lysosomal degradation, further highlighting the important role of LAP in antiviral immunity and providing a theoretical basis and experimental support for the development of new antiviral strategies.

Indexed as

InterferonsLysosomesMicrotubule-Associated ProteinsPhagocytosisPicornaviridae InfectionsAnimalsAutophagyCell LineChlorocebus aethiopsFoot-and-Mouth Disease VirusImmunity, InnateMiceMice, Inbred C57BLMice, KnockoutPicornaviridaeVero CellsInterferonsMap1lc3b protein, mouseMicrotubule-Associated ProteinsCanonical autophagyCRISPR/Cas9Innate immune responseSingle-membrane phagosomesVISA

Identifiers

PMID42017991
PMCPMC13237333

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LicenceCC BY-NC-ND
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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.