Evidence map›Paper›PMID 32532301›Full record

ArticleVirology journal2020

Influenza a virus antagonizes type I and type II interferon responses via SOCS1-dependent ubiquitination and degradation of JAK1.

Yinping Du, Fan Yang, Qiuxia Wang, Nuo Xu, Yizhang Xie, Sujuan Chen, Tao Qin, Daxin Peng

Open access · goldAbstract read
In one paragraph

Article in Virology journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.8field-weighted citation impact, top 12% of its field
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

25 citing papers in PubMed, 37 citations in OpenAlex.

  1. Anellovirus-mediated interferon dysregulation enhances virus-induced lung injury.American journal of respiratory cell and molecular biology · 2026
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  17. The Roles of Ubiquitination in Pathogenesis of Influenza Virus Infection.International journal of molecular sciences · 2022
    Review
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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

8 authors at 2 institutions in 1 country.

Yinping DuCollege of Veterinary Medicine, Yangzhou University, Yangzhou, Jiangsu, 225009, People's Republic of China.
Fan YangCollege of Veterinary Medicine, Yangzhou University, Yangzhou, Jiangsu, 225009, People's Republic of China.
Qiuxia WangCollege of Veterinary Medicine, Yangzhou University, Yangzhou, Jiangsu, 225009, People's Republic of China.
Nuo XuCollege of Veterinary Medicine, Yangzhou University, Yangzhou, Jiangsu, 225009, People's Republic of China.
Yizhang XieCollege of Veterinary Medicine, Yangzhou University, Yangzhou, Jiangsu, 225009, People's Republic of China.
Sujuan ChenCollege of Veterinary Medicine, Yangzhou University, Yangzhou, Jiangsu, 225009, People's Republic of China.
Tao QinCollege of Veterinary Medicine, Yangzhou University, Yangzhou, Jiangsu, 225009, People's Republic of China.
Daxin PengCollege of Veterinary Medicine, Yangzhou University, Yangzhou, Jiangsu, 225009, People's Republic of China. pengdx@yzu.edu.cn.ORCID 0000-0001-6773-5149
Jiangsu Provincial Center for Disease Control and Prevention · CNChina Animal Disease Control Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlthough influenza A virus (IAV) employs diverse strategies to evade IFN responses by inhibiting the synthesis of IFN, how IAV regulates signaling downstream of IFN is incompletely understood.

methodsIn this study, we used Western blot-based protein analysis coupled with RT-qPCR, overexpression and RNA interference to investigate the regulation of JAK1 by IAV infection.

resultsThe results indicated that JAK1 was ubiquitinated and degraded, resulting in inhibition of type I and type II IFN responses, demonstrating that IAV antagonizes the IFN-activated JAK/STAT signaling pathway by inducing the degradation of JAK1. Furthermore. IAV infection upregulated the suppressor of cytokine signaling (SOCS) protein SOCS1, and SOCS1 mediated the ubiquitination and degradation of JAK1.

conclusionCollectively, our findings suggest that IAV infection induces SOCS1 expression to promote JAK1 degradation, which in turn inhibits host innate immune responses.

Indexed as

A549 CellsDown-RegulationHEK293 CellsHost Microbial InteractionsHumansImmune EvasionImmunity, InnateInfluenza A virusInterferon-gammaInterferon Type IJanus Kinase 1Signal TransductionSuppressor of Cytokine Signaling 1 ProteinUbiquitinationInterferon-gammaInterferon Type IJAK1 protein, humanJanus Kinase 1SOCS1 protein, humanSuppressor of Cytokine Signaling 1 ProteinDegradationIAVIFNJAK1SOCS1

Identifiers

PMID32532301
PMCPMC7291424
OpenAlexW3035732289

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.