Evidence map›Paper›PMID 33352639›Full record

ArticleInternational journal of molecular sciences2020

Dengue Nonstructural Protein 1 Maintains Autophagy through Retarding Caspase-Mediated Cleavage of Beclin-1.

Zi-Yi Lu, Miao-Huei Cheng, Chia-Yi Yu, Yee-Shin Lin, Trai-Ming Yeh, Chia-Ling Chen, Chien-Chin Chen, Shu-Wen Wan, Chih-Peng Chang

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
21.4field-weighted citation impact, top 1% 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

14 citing papers in PubMed, 127 citations in OpenAlex.

  1. A gut commensalVirulence · 2026
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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

9 authors at 4 institutions in 1 country.

Zi-Yi LuDepartment of Microbiology and Immunology, College of Medicine, National Cheng Kung University, Tainan 701, Taiwan.
Miao-Huei ChengSchool of Medicine for International Students, College of Medicine, I-Shou University, Kaohsiung 824, Taiwan.
Chia-Yi YuNational Institute of Infectious Diseases and Vaccinology, National Health Research Institutes, Miaoli 350, Taiwan.
Yee-Shin LinDepartment of Microbiology and Immunology, College of Medicine, National Cheng Kung University, Tainan 701, Taiwan.
Trai-Ming YehCenter of Infectious Disease and Signaling Research, National Cheng Kung University, Tainan 701, Taiwan.
Chia-Ling ChenSchool of Respiratory Therapy, College of Medicine, Taipei Medical University, Taipei 110, Taiwan.
Chien-Chin ChenDepartment of Pathology, Ditmanson Medical Foundation Chia-Yi Christian Hospital, Chiayi 600, Taiwan.ORCID 0000-0001-9599-0884
Shu-Wen WanSchool of Medicine for International Students, College of Medicine, I-Shou University, Kaohsiung 824, Taiwan.
Chih-Peng ChangDepartment of Microbiology and Immunology, College of Medicine, National Cheng Kung University, Tainan 701, Taiwan.
National Cheng Kung University · TWChia-Yi Christian Hospital · TWI-Shou University · TWNational Health Research Institutes · TW

Funding

The Ministry of Science and Technology, Taiwan MOST 104-2320-B-006 -038 -MY3, MOST 108-2320-B-214-007 and MOST 109-2320-B-214-004The National Health Research Institutes, Taiwan NHRI-109A1-MRCO-02202013
6 · The paper itself

Abstract

Dengue virus (DENV) infection is a significant public health threat in tropical and subtropical regions; however, there is no specific antiviral drug. Accumulated studies have revealed that DENV infection induces several cellular responses, including autophagy and apoptosis. The crosstalk between autophagy and apoptosis is associated with the interactions among components of these two pathways, such as apoptotic caspase-mediated cleavage of autophagy-related proteins. Here, we show that DENV-induced autophagy inhibits early cell apoptosis and hence enhances DENV replication. Later, the apoptotic activities are elevated to suppress autophagy through cleavage of Beclin-1, an essential autophagy-related protein. Inhibition of cleavage of Beclin-1 by a pan-caspase inhibitor, Z-VAD, increases both autophagy and viral replication. Regarding the mechanism, we further found that DENV nonstructural protein 1 (NS1) is able to interact with Beclin-1 during DENV infection. The interaction between Beclin-1 and NS1 attenuates Beclin-1 cleavage and facilitates autophagy to prevent cell apoptosis. Our study suggests a novel mechanism whereby NS1 preserves Beclin-1 for maintaining autophagy to antagonize early cell apoptosis; however, elevated caspases trigger apoptosis by degrading Beclin-1 in the late stage of infection. These findings suggest implications for anti-DENV drug design.

Indexed as

A549 CellsAedesAnimalsAutophagyBeclin-1CaspasesDengueDengue VirusHumansViral Nonstructural ProteinsBeclin-1CaspasesViral Nonstructural ProteinsapoptosisautophagyBeclin-1caspasedengue virusNS1

Identifiers

PMID33352639
PMCPMC7766445
OpenAlexW3111215165

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.