Evidence map›Paper›PMID 32117097›Full record

ArticleFrontiers in microbiology2020

Coxsackievirus A6 Induces Necroptosis for Viral Production.

Shuxia Zhang, Xiaoyan Yu, Xiangling Meng, Wenbo Huo, Ying Su, Jinming Liu, Yumeng Liu, Jun Zhang, Shaohua Wang, Jinghua Yu

Open access · goldAbstract read
In one paragraph

Article in Frontiers in microbiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 21% 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

11 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Necroptosis in CNS diseases: Focus on astrocytes.Frontiers in aging neuroscience · 2022
    Review
  11. Caspase-3 inhibitor inhibits enterovirus D68 production.Journal of microbiology (Seoul, Korea) · 2020
    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

10 authors at 2 institutions in 1 country.

Shuxia ZhangDepartment of Experimental Pharmacology and Toxicology, School of Pharmaceutical Science, Jilin University, Changchun, China.
Xiaoyan YuDepartment of Experimental Pharmacology and Toxicology, School of Pharmaceutical Science, Jilin University, Changchun, China.
Xiangling MengDepartment of Experimental Pharmacology and Toxicology, School of Pharmaceutical Science, Jilin University, Changchun, China.
Wenbo HuoDepartment of Experimental Pharmacology and Toxicology, School of Pharmaceutical Science, Jilin University, Changchun, China.
Ying SuDepartment of Experimental Pharmacology and Toxicology, School of Pharmaceutical Science, Jilin University, Changchun, China.
Jinming LiuDepartment of Experimental Pharmacology and Toxicology, School of Pharmaceutical Science, Jilin University, Changchun, China.
Yumeng LiuDepartment of Experimental Pharmacology and Toxicology, School of Pharmaceutical Science, Jilin University, Changchun, China.
Jun ZhangInstitute of Virology and AIDS Research, The First Hospital of Jilin University, Jilin University, Changchun, China.
Shaohua WangInstitute of Virology and AIDS Research, The First Hospital of Jilin University, Jilin University, Changchun, China.
Jinghua YuInstitute of Virology and AIDS Research, The First Hospital of Jilin University, Jilin University, Changchun, China.
Jilin University · CNFirst Hospital of Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hand, foot, and mouth disease (HFMD) is a febrile exanthematous disease with typical or atypical symptoms. Typical HFMD is usually caused by enterovirus 71 (EV71) or coxsackievirus A16, while atypical HFMD is usually caused by coxsackievirus A6 (CA6). In recent years, worldwide outbreaks of CA6-associated HFMD have dramatically increased, although the pathogenic mechanism of CA6 is still unclear. EV71 has been established to induce caspase-dependent apoptosis, but in this study, we demonstrate that CA6 infection promotes a distinct pathway of cell death that involves loss of cell membrane integrity. Necrostatin-1, an inhibitor of necroptosis, blocks the cell death induced by CA6 infection, but Z-DEVD-FMK, an inhibitor of caspase-3, has no effect on CA6-induced cell death. Furthermore, CA6 infection up-regulates the expression of the necroptosis signaling molecule RIPK3. Importantly, necrostatin-1 inhibits CA6 viral production, as assessed by its ability to inhibit levels of VP1 protein and genomic RNA and infectious particles. CA6-induced necroptosis is not dependent on the generation of reactive oxygen species; however, viral 3D protein can directly bind RIPK3, which is suggestive of a direct mechanism of necroptosis induction. Therefore, these results indicate that CA6 induces a mechanism of RIPK3-dependent necroptosis for viral production that is distinct from the mechanism of apoptosis induced by typical HFMD viruses.

Indexed as

CA6host–pathogen interactionnecroptosisRIPK3viral production

Identifiers

PMID32117097
PMCPMC7011610
OpenAlexW3004638230

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.