Evidence map›Paper›PMID 28229049›Full record

ArticleFrontiers in cellular and infection microbiology2017

Human Enterovirus 68 Interferes with the Host Cell Cycle to Facilitate Viral Production.

Zeng-Yan Wang, Ting Zhong, Yue Wang, Feng-Mei Song, Xiao-Feng Yu, Li-Ping Xing, Wen-Yan Zhang, Jing-Hua Yu, Shu-Cheng Hua, Xiao-Fang Yu

Abstract read
In one paragraph

Article in Frontiers in cellular and infection microbiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing 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

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

27 citing papers in PubMed.

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  15. Caspase-3 inhibitor inhibits enterovirus D68 production.Journal of microbiology (Seoul, Korea) · 2020
    Article
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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.

Zeng-Yan WangDepartment of Internal Medicine, The First Hospital of Jilin University, Jilin University Changchun, China.
Ting ZhongMedicinal Chemistry, College of Pharmacy, Changchun University of Chinese Medicine Changchun, China.
Yue WangChemistry of Traditional Chinese Medicine, College of Pharmacy, Changchun University of Chinese Medicine Changchun, China.
Feng-Mei SongDepartment of Experimental Pharmacology and Toxicology, School of Pharmacy, Jilin Univrsity Changchun, China.
Xiao-Feng YuInstitute of Virology and AIDS Research, The First Hospital of Jilin University, Jilin University Changchun, China.
Li-Ping XingDepartment of Internal Medicine, The First Hospital of Jilin University, Jilin University Changchun, China.
Wen-Yan ZhangInstitute of Virology and AIDS Research, The First Hospital of Jilin University, Jilin University Changchun, China.
Jing-Hua YuInstitute of Virology and AIDS Research, The First Hospital of Jilin University, Jilin University Changchun, China.
Shu-Cheng HuaDepartment of Internal Medicine, The First Hospital of Jilin University, Jilin University Changchun, China.
Xiao-Fang YuInstitute of Virology and AIDS Research, The First Hospital of Jilin University, Jilin University Changchun, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Enterovirus D68 (EV-D68) is an emerging pathogen that recently caused a large outbreak of severe respiratory disease in the United States and other countries. Little is known about the relationship between EV-D68 virus and host cells. In this study, we assessed the effect of the host cell cycle on EV-D68 viral production, as well as the ability of EV-D68 to manipulate host cell cycle progression. The results suggest that synchronization in G0/G1 phase, but not S phase, promotes viral production, while synchronization in G2/M inhibits viral production. Both an early EV-D68 isolate and currently circulating strains of EV-D68 can manipulate the host cell cycle to arrest cells in the G0/G1 phase, thus providing favorable conditions for virus production. Cell cycle regulation by EV-D68 was associated with corresponding effects on the expression of cyclins and CDKs, which were observed at the level of the protein and/or mRNA. Furthermore, the viral non-structural protein 3D of EV-D68 prevents progression from G0/G1 to S. Interestingly, another member of the

Indexed as

Cell CycleVirus ReplicationCell Cycle CheckpointsCell LineCells, CulturedEnterovirus D, HumanEnterovirus InfectionsHost-Pathogen InteractionsHumanscell cycleenterovirus 68 (EV-D68)G0/G1 arresthost-pathogen interactionviral replication

Identifiers

PMID28229049
PMCPMC5296350

What OpenQuestion holds

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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.