Evidence map›Paper›PMID 32149091›Full record

ArticleBioMed research international2020

Induction of SOCS Expression by EV71 Infection Promotes EV71 Replication.

Wenying Gao, Min Hou, Xin Liu, Zhaolong Li, Yongjun Yang, Wenyan Zhang

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

14 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Review
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  8. Food chemistry: X · 2022
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Frontiers in cellular and infection microbiology · 2021
    Article
  14. Article
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

6 authors at 1 institution in 1 country.

Wenying GaoThe First Hospital of Jilin University, Institute of Virology and AIDS Research & Key Laboratory of Zoonosis, Ministry of Education, College of Veterinary Medicine, Jilin University, Changchun 130021, China.
Min HouThe First Hospital of Jilin University, Institute of Virology and AIDS Research & Key Laboratory of Zoonosis, Ministry of Education, College of Veterinary Medicine, Jilin University, Changchun 130021, China.
Xin LiuThe First Hospital of Jilin University, Institute of Virology and AIDS Research & Key Laboratory of Zoonosis, Ministry of Education, College of Veterinary Medicine, Jilin University, Changchun 130021, China.
Zhaolong LiThe First Hospital of Jilin University, Institute of Virology and AIDS Research & Key Laboratory of Zoonosis, Ministry of Education, College of Veterinary Medicine, Jilin University, Changchun 130021, China.
Yongjun YangThe First Hospital of Jilin University, Institute of Virology and AIDS Research & Key Laboratory of Zoonosis, Ministry of Education, College of Veterinary Medicine, Jilin University, Changchun 130021, China.ORCID https://orcid.org/0000-0002-5294-9790
Wenyan ZhangThe First Hospital of Jilin University, Institute of Virology and AIDS Research & Key Laboratory of Zoonosis, Ministry of Education, College of Veterinary Medicine, Jilin University, Changchun 130021, China.ORCID https://orcid.org/0000-0003-4507-521X
Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Enterovirus 71 (EV71) is the causative pathogen of hand, foot, and mouth disease (HFMD). However, no effective antiviral therapy is currently available. Some viruses could escape the host's innate immunity by upregulating suppressor of cytokine signaling (SOCS) proteins. Until now, whether EV71 evades the host immune system by regulating the expression of SOCS proteins remains unknown. In this study, we found that EV71 infection promoted SOCS expression at both mRNA and protein levels in vitro and in vivo. Consistently, the infectivity of EV71 was decreased significantly in the SOCS3 or SOCS1 knockdown cells, suggesting that SOCS1 and especially SOCS3 are crucial for EV71 infection. Further investigation showed that SOCS3 promoted virus infection by inhibiting interferon-induced STAT3 phosphorylation. SOCS1 and SOCS3 mRNA expressions were independent on virus-induced type I interferon expression but were blocked by the inhibitor of NF-

Indexed as

AnimalsDisease Models, AnimalEnterovirusEnterovirus InfectionsImmunity, InnateInterferon Type IMiceMice, KnockoutNF-kappa BReceptor, Interferon alpha-betaRNA, MessengerSuppressor of Cytokine Signaling 1 ProteinSuppressor of Cytokine Signaling 3 ProteinSuppressor of Cytokine Signaling ProteinsUp-RegulationVirus ReplicationIfnar1 protein, mouseInterferon Type INF-kappa BReceptor, Interferon alpha-betaRNA, MessengerSuppressor of Cytokine Signaling 1 ProteinSuppressor of Cytokine Signaling 3 ProteinSuppressor of Cytokine Signaling Proteins

Identifiers

PMID32149091
PMCPMC7054758
OpenAlexW3007458739

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.