Evidence map›Paper›PMID 32603377›Full record

ArticlePLoS pathogens2020

Newcastle Disease virus infection activates PI3K/Akt/mTOR and p38 MAPK/Mnk1 pathways to benefit viral mRNA translation via interaction of the viral NP protein and host eIF4E.

Yuan Zhan, Shengqing Yu, Shen Yang, Xusheng Qiu, Chunchun Meng, Lei Tan, Cuiping Song, Ying Liao, Weiwei Liu, Yingjie Sun and 1 more

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
7.9field-weighted citation impact, top 2% 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

46 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.

  1. Pooled it
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  4. CMGC Kinases in Viral Infection and Human Disease.Pathogens (Basel, Switzerland) · 2026
    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

11 authors at 1 institution in 1 country.

Yuan ZhanShanghai Veterinary Research Institute, Chinese Academy of Agricultural Science, Shanghai, P.R. China.
Shengqing YuShanghai Veterinary Research Institute, Chinese Academy of Agricultural Science, Shanghai, P.R. China.
Shen YangShanghai Veterinary Research Institute, Chinese Academy of Agricultural Science, Shanghai, P.R. China.
Xusheng QiuShanghai Veterinary Research Institute, Chinese Academy of Agricultural Science, Shanghai, P.R. China.
Chunchun MengShanghai Veterinary Research Institute, Chinese Academy of Agricultural Science, Shanghai, P.R. China.
Lei TanShanghai Veterinary Research Institute, Chinese Academy of Agricultural Science, Shanghai, P.R. China.
Cuiping SongShanghai Veterinary Research Institute, Chinese Academy of Agricultural Science, Shanghai, P.R. China.
Ying LiaoShanghai Veterinary Research Institute, Chinese Academy of Agricultural Science, Shanghai, P.R. China.
Weiwei LiuShanghai Veterinary Research Institute, Chinese Academy of Agricultural Science, Shanghai, P.R. China.
Yingjie SunShanghai Veterinary Research Institute, Chinese Academy of Agricultural Science, Shanghai, P.R. China.
Chan DingShanghai Veterinary Research Institute, Chinese Academy of Agricultural Science, Shanghai, P.R. China.ORCID 0000-0003-0216-2129
Shanghai Veterinary Research Institute · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Newcastle disease virus (NDV), a member of the Paramyxoviridae family, can activate PKR/eIF2α signaling cascade to shutoff host and facilitate viral mRNA translation during infection, however, the mechanism remains unclear. In this study, we revealed that NDV infection up-regulated host cap-dependent translation machinery by activating PI3K/Akt/mTOR and p38 MAPK/Mnk1 pathways. In addition, NDV infection induced p38 MAPK/Mnk1 signaling participated 4E-BP1 hyperphosphorylation for efficient viral protein synthesis when mTOR signaling is inhibited. Furthermore, NDV NP protein was found to be important for selective cap-dependent translation of viral mRNAs through binding to eIF4E during NDV infection. Taken together, NDV infection activated multiple signaling pathways for selective viral protein synthesis in infected cells, via interaction between viral NP protein and host translation machinery. Our results may help to design novel targets for therapeutic intervention against NDV infection and to understand the NDV anti-oncolytic mechanism.

Indexed as

Avian ProteinsEukaryotic Initiation Factor-4EMAP Kinase Signaling SystemNewcastle disease virusNucleoproteinsRNA, MessengerRNA, ViralViral ProteinsAnimalsChick EmbryoChickensHEK293 CellsHeLa CellsHumansIntracellular Signaling Peptides and ProteinsNucleocapsid ProteinsAvian ProteinsEIF4E protein, humanEukaryotic Initiation Factor-4EIntracellular Signaling Peptides and ProteinsMKNK1 protein, humanMTOR protein, humanNucleocapsid Proteinsnucleoprotein, Newcastle disease virusNucleoproteinsp38 Mitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktRNA, MessengerRNA, ViralTOR Serine-Threonine KinasesViral Proteins

Identifiers

PMID32603377
PMCPMC7326156
OpenAlexW3039609329

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.