Evidence map›Paper›PMID 40137969›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2025

MiR-362-3p mediates IFNα-induced antiviral viability against Enterovirus 71 (EV71).

San Wang, Lan Chen, Zongtao Wu, Yingbo Zou, Yunrong Li, Xiang He, Yusong Zhang, Bo Huang

Abstract read
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In one paragraph

Article in Naunyn-Schmiedeberg's archives of pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

8 authors.

San WangDepartment of Pediatrics, The Third Affiliated Hospital of Zunyi Medical University, the First People'S Hospital of Zunyi), Guizhou, 563099, China.
Lan ChenDepartment of Pediatrics, The Third Affiliated Hospital of Zunyi Medical University, the First People'S Hospital of Zunyi), Guizhou, 563099, China.
Zongtao WuDepartment of Pediatrics, The Third Affiliated Hospital of Zunyi Medical University, the First People'S Hospital of Zunyi), Guizhou, 563099, China.
Yingbo ZouDepartment of Pediatrics, The Third Affiliated Hospital of Zunyi Medical University, the First People'S Hospital of Zunyi), Guizhou, 563099, China.
Yunrong LiDepartment of Pediatrics, The Third Affiliated Hospital of Zunyi Medical University, the First People'S Hospital of Zunyi), Guizhou, 563099, China.
Xiang HeDepartment of Pediatrics, The Third Affiliated Hospital of Zunyi Medical University, the First People'S Hospital of Zunyi), Guizhou, 563099, China.
Yusong ZhangDepartment of Pediatrics, The Third Affiliated Hospital of Zunyi Medical University, the First People'S Hospital of Zunyi), Guizhou, 563099, China.
Bo HuangDepartment of Pediatrics, The Third Affiliated Hospital of Zunyi Medical University, the First People'S Hospital of Zunyi), Guizhou, 563099, China. hbhcw212@126.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Enteroviruses, which belong to the Picornaviridae family, include species that infect humans and Interferon Alpha (IFNα) is commonly used against Enterovirus 71 (EV71) infections. This study investigated the role of IFNα-induced miR-362-3p expression in the defense against EV71EV71. Differential analysis identified up-regulated miRNAs following IFNα treatment. RD cells were used to assess EV71proliferation, while HMC3 cells were employed to evaluate the effects of IFNα and EV71 on miR-362-3p expression. Antiviral activity was assessed by modulating miR-362-3p levels. Compared to the NC mimic group, miR-362-3p in miR-362-3p mimic and IFNα treatment groups was increased; cell viability was enhanced; -lgTCID50 was reduced, and the replication of EV71 was inhibited. Further, VP1 mRNA and protein expression declined significantly in miR-362-3p mimic group vs NC mimic while they were notably elevated in the miR-362-3p inhibitor group vs NC inhibitor. IFNα treatment could induce miR-362-3p production and enhanced cell viability in HMC3 cells. Besides, when compared with the miR-362-3p mimic group, IFNα combined with miR-362-3p mimic group reduced -lgTCID50 and significantly decreased the expression of VP1 mRNA and protein. Conclusion: The inhibition of EV71-infected HMC3 cell replication was related to the upregulation of miR-362-3p induced by IFNα, which in turn enhanced antiviral viability.

Indexed as

Antiviral AgentsEnterovirus A, HumanInterferon-alphaMicroRNAsCell LineCell SurvivalEnterovirus InfectionsHumansVirus ReplicationAntiviral AgentsInterferon-alphaMicroRNAsAntiviral activityEnterovirus 71HMC3 cellsIFNαMiR-362-3p

Identifiers

PMID40137969

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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.