Evidence map›Paper›PMID 35972295›Full record

ArticleJournal of virology2022

African Swine Fever Virus pI215L Inhibits Type I Interferon Signaling by Targeting Interferon Regulatory Factor 9 for Autophagic Degradation.

Liang Li, Jiyang Fu, Jixuan Li, Shibang Guo, Qichao Chen, Yibo Zhang, Zhankui Liu, Chen Tan, Huanchun Chen, Xiangru Wang

Open access · hybridAbstract read
In one paragraph

Article in Journal of virology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
9.7field-weighted citation impact, top 1% 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

32 citing papers in PubMed, 45 citations in OpenAlex.

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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

10 authors at 1 institution in 1 country.

Liang LiState Key Laboratory of Agricultural Microbiology, College of Veterinary Medicine, Huazhong Agricultural Universitygrid.35155.37, Wuhan, China.
Jiyang FuState Key Laboratory of Agricultural Microbiology, College of Veterinary Medicine, Huazhong Agricultural Universitygrid.35155.37, Wuhan, China.
Jixuan LiState Key Laboratory of Agricultural Microbiology, College of Veterinary Medicine, Huazhong Agricultural Universitygrid.35155.37, Wuhan, China.
Shibang GuoState Key Laboratory of Agricultural Microbiology, College of Veterinary Medicine, Huazhong Agricultural Universitygrid.35155.37, Wuhan, China.
Qichao ChenState Key Laboratory of Agricultural Microbiology, College of Veterinary Medicine, Huazhong Agricultural Universitygrid.35155.37, Wuhan, China.
Yibo ZhangState Key Laboratory of Agricultural Microbiology, College of Veterinary Medicine, Huazhong Agricultural Universitygrid.35155.37, Wuhan, China.
Zhankui LiuState Key Laboratory of Agricultural Microbiology, College of Veterinary Medicine, Huazhong Agricultural Universitygrid.35155.37, Wuhan, China.
Chen TanState Key Laboratory of Agricultural Microbiology, College of Veterinary Medicine, Huazhong Agricultural Universitygrid.35155.37, Wuhan, China.ORCID 0000-0003-4622-4483
Huanchun ChenState Key Laboratory of Agricultural Microbiology, College of Veterinary Medicine, Huazhong Agricultural Universitygrid.35155.37, Wuhan, China.
Xiangru WangState Key Laboratory of Agricultural Microbiology, College of Veterinary Medicine, Huazhong Agricultural Universitygrid.35155.37, Wuhan, China.ORCID 0000-0003-0191-1378
Huazhong Agricultural University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

African swine fever virus (ASFV) is the etiological agent of a highly lethal hemorrhagic disease in domestic pigs and wild boars that has significant economic consequences for the pig industry. The type I interferon (IFN) signaling pathway is a pivotal component of the innate antiviral response, and ASFV has evolved multiple mechanisms to antagonize this pathway and facilitate infection. Here, we reported a novel function of ASFV pI215L in inhibiting type I IFN signaling. Our results showed that ASFV pI215L inhibited IFN-stimulated response element (ISRE) promoter activity and subsequent transcription of IFN-stimulated genes (ISGs) by triggering interferon regulatory factor 9 (IRF9) degradation. Additionally, we found that catalytically inactive pI215L mutations retained the ability to block type I IFN signaling, indicating that this only known viral E2 ubiquitin-conjugating enzyme mediates IFR9 degradation in a ubiquitin-conjugating activity-independent manner. By coimmunoprecipitation, confocal immunofluorescence, and subcellular fractionation approaches, we demonstrated that pI215L interacted with IRF9 and impaired the formation and nuclear translocation of IFN-stimulated gene factor 3 (ISGF3). Moreover, further mechanism studies supported that pI215L induced IRF9 degradation through the autophagy-lysosome pathway in both pI215L-overexpressed and ASFV-infected cells. These findings reveal a new immune evasion strategy evolved by ASFV in which pI215L acts to degrade host IRF9 via the autophagic pathway, thus inhibiting the type I IFN signaling and counteracting the host innate immune response.

Indexed as

African Swine FeverAutophagyInterferon-Stimulated Gene Factor 3, gamma SubunitInterferon Type IAfrican Swine Fever VirusAnimalsImmunity, InnateSignal TransductionSus scrofaSwineUbiquitin-Conjugating EnzymesInterferon-Stimulated Gene Factor 3, gamma SubunitInterferon Type IUbiquitin-Conjugating EnzymesAfrican swine fever virusautophagyIRF9pI215Ltype I IFN signaling

Identifiers

PMID35972295
PMCPMC9472647
OpenAlexW4293063668

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.