Evidence map›Paper›PMID 29703921›Full record

ArticleScientific reports2018

Mutations in VP1 and 5'-UTR affect enterovirus 71 virulence.

Ching-Kun Chang, Shang-Rung Wu, Ying-Chin Chen, Kuen-Jin Lee, Nai-Hsiang Chung, Yi-Ju Lu, Shu-Ling Yu, Chia-Chyi Liu, Yen-Hung Chow

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

16 citing papers in PubMed, 22 citations in OpenAlex.

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  11. Cellular receptors for enterovirus A71.Journal of biomedical science · 2020
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 1 country.

Ching-Kun ChangNational Institute of Infectious Disease and Vaccinology, National Health Research Institutes, Zhunan, 350, Taiwan.
Shang-Rung WuInstitute of Oral Medicine, National Cheng Kung University, Tainan, 701, Taiwan.
Ying-Chin ChenNational Institute of Infectious Disease and Vaccinology, National Health Research Institutes, Zhunan, 350, Taiwan.
Kuen-Jin LeeInstitute of Oral Medicine, National Cheng Kung University, Tainan, 701, Taiwan.
Nai-Hsiang ChungNational Institute of Infectious Disease and Vaccinology, National Health Research Institutes, Zhunan, 350, Taiwan.
Yi-Ju LuNational Institute of Infectious Disease and Vaccinology, National Health Research Institutes, Zhunan, 350, Taiwan.
Shu-Ling YuNational Institute of Infectious Disease and Vaccinology, National Health Research Institutes, Zhunan, 350, Taiwan.
Chia-Chyi LiuNational Institute of Infectious Disease and Vaccinology, National Health Research Institutes, Zhunan, 350, Taiwan.
Yen-Hung ChowNational Institute of Infectious Disease and Vaccinology, National Health Research Institutes, Zhunan, 350, Taiwan. choeyenh@nhri.org.tw.
National Health Research Institutes · TWNational Cheng Kung University · TWNational Defense Medical Center · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Enterovirus 71 (EV71) is a major cause of hand, foot and mouth disease (HFMD). The current EV71 propagating in Vero (EV-V) or sub-passaged in RD (EV-R) cells was used as a pathogen. Interestingly, EV-R exhibited differential virulence; challenging human scavenger receptor class B2-expressing (hSCARB2-Tg) mice with EV71 revealed that EV-V was more virulent than EV-R: 100% of mice that received lethal amounts of EV-V died, while all the mice that received EV-R survived. Severe pathogenesis correlated with viral burdens and proinflammatory cytokine levels were observed in EV-V-challenged mice, but controversy in EV-R-challenged mice. Consensus sequence analysis revealed EV-R rapidly acquired complete mutations at E145G and S241L and partial mutations at V146I of VP1, and acquired a T to C substitution at nucleotide 494 of the 5'-UTR. EV-R exhibited higher binding affinity for another EV71 receptor, human P-selectin glycoprotein ligand-1 (hPSGL-1), than EV-V. Both EV71s exhibited no significant difference in binding to hSCARB2. The molecular modelling indicate that these mutations might influence EV71 engagement with PSGL-1 and in vivo virulence.

Indexed as

5' Untranslated RegionsMutationAnimalsCell LineChlorocebus aethiopsCytokinesDisease Models, AnimalDNA Mutational AnalysisEnterovirus A, HumanEnterovirus InfectionsHumansMembrane GlycoproteinsMiceReceptors, VirusSurvival AnalysisViral Load5' Untranslated RegionsCytokinesMembrane GlycoproteinsP-selectin ligand proteinReceptors, Virusviral protein 1, rhinovirusViral ProteinsViral Structural Proteins

Identifiers

PMID29703921
PMCPMC5923339
OpenAlexW2805667693

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.