Evidence map›Paper›PMID 31319897›Full record

ArticleVirology journal2019

The effects of autophagy on the replication of Nelson Bay orthoreovirus.

Xiao-Li Tao, Wei Zhao, Wei Tong, Xiao-Fang Wang, Li-Li Dou, Jiang-Man Chen, Nian Liu, Ying Lu, Yi-Bo Zhang, Xu-Peng Jin and 4 more

Open access · goldAbstract read
In one paragraph

Article in Virology journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.2field-weighted citation impact, top 45% 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

0 citing papers in PubMed, 4 citations in OpenAlex.

No citing paper in PubMed yet.

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

14 authors at 2 institutions in 1 country.

Xiao-Li TaoDepartment of Pathogenic Microbiology, College of Basic Medical Sciences, China Medical University, No. 77, Puhe Road, Shenyang North New Area, Shenyang City, 110013, Liaoning Province, People's Republic of China.
Wei ZhaoDepartment of Pathogenic Microbiology, College of Basic Medical Sciences, Jinzhou Medical University, No. 40, the Third Section of SongPo Rd, Jinzhou City, 121200, Liaoning Province, China.
Wei TongDepartment of Pathogenic Microbiology, College of Basic Medical Sciences, Jinzhou Medical University, No. 40, the Third Section of SongPo Rd, Jinzhou City, 121200, Liaoning Province, China.
Xiao-Fang WangDepartment of Pathogenic Microbiology, College of Basic Medical Sciences, Jinzhou Medical University, No. 40, the Third Section of SongPo Rd, Jinzhou City, 121200, Liaoning Province, China.
Li-Li DouDepartment of Pathogenic Microbiology, College of Basic Medical Sciences, Jinzhou Medical University, No. 40, the Third Section of SongPo Rd, Jinzhou City, 121200, Liaoning Province, China.
Jiang-Man ChenDepartment of Pathogenic Microbiology, College of Basic Medical Sciences, Jinzhou Medical University, No. 40, the Third Section of SongPo Rd, Jinzhou City, 121200, Liaoning Province, China.
Nian LiuDepartment of Pathogenic Microbiology, College of Basic Medical Sciences, Jinzhou Medical University, No. 40, the Third Section of SongPo Rd, Jinzhou City, 121200, Liaoning Province, China.
Ying LuDepartment of Pathogenic Microbiology, College of Basic Medical Sciences, Jinzhou Medical University, No. 40, the Third Section of SongPo Rd, Jinzhou City, 121200, Liaoning Province, China.
Yi-Bo ZhangDepartment of Pathogenic Microbiology, College of Basic Medical Sciences, Jinzhou Medical University, No. 40, the Third Section of SongPo Rd, Jinzhou City, 121200, Liaoning Province, China.
Xu-Peng JinDepartment of Pathogenic Microbiology, College of Basic Medical Sciences, Jinzhou Medical University, No. 40, the Third Section of SongPo Rd, Jinzhou City, 121200, Liaoning Province, China.
Yan-Fei ShenDepartment of Pathogenic Microbiology, College of Basic Medical Sciences, Jinzhou Medical University, No. 40, the Third Section of SongPo Rd, Jinzhou City, 121200, Liaoning Province, China.
Hong-Yan ZhaoDepartment of Pathogenic Microbiology, College of Basic Medical Sciences, Jinzhou Medical University, No. 40, the Third Section of SongPo Rd, Jinzhou City, 121200, Liaoning Province, China.
Hong JinDepartment of Pathogenic Microbiology, College of Basic Medical Sciences, China Medical University, No. 77, Puhe Road, Shenyang North New Area, Shenyang City, 110013, Liaoning Province, People's Republic of China. jinhongf@sina.com.
Yong-Gang LiDepartment of Pathogenic Microbiology, College of Basic Medical Sciences, Jinzhou Medical University, No. 40, the Third Section of SongPo Rd, Jinzhou City, 121200, Liaoning Province, China. lygjo@hotmail.com.
Jinzhou Medical University · CNChina Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNelson Bay orthoreovirus (NBV) was first isolated over 40 years ago from a fruit bat in Australia. Normally, NBV does not cause human diseases, but recently several NBV strains have been associated with human respiratory tract infections, thus attracting clinical attention. Autophagy, an evolutionarily conserved process in eukaryotic cells, degrades intracellular substrates, participates in multiple physiological processes, and maintains cellular homeostasis. In addition, autophagy is intimately involved in viral infection.

methodsA new strain of NBV, isolated from a patient with a respiratory tract infection who returned to Japan from Bali, Indonesia, in 2007, was used in this study. NBV was rescued using a reverse genetics system involving cotransfection of BHK cells with 11 plasmids (pT7-L1 MB, pT7-L2 MB, pT7-L3 MB, pT7-M1 MB, pT7-M2 MB, pT7-M3 MB, pT7-S1 MB, pT7-S2 MB, pT7-S3 MB, pT7-S4 MB, and pcDNA3.1-T7), yielding NBV-MB. Recovered viruses were confirmed by immunofluorescence. The effect of NBV-MB on autophagy was evaluated by measuring the LC3-I/II proteins by immunoblot analysis after infection of BHK cells. Furthermore, after treatment with rapamycin (RAPA), 3-methyladenine (3-MA), chloroquine (CQ), or plasmid (GFP-LC3) transfection, the changes in expression of the LC3 gene and the amount of LC3-I/II protein were examined. In addition, variations in viral titer were assayed after treatment of BHK cells with drugs or after transfection with plasmids pCAGM3 and pCAGS3, which encode virus nonstructural proteins μNS and σNS, respectively.

resultsNBV-MB infection induced autophagy in host cells; however, the level of induction was dependent on viral replication. Induction of autophagy increased viral replication. By contrast, inhibiting autophagy suppressed NBV replication, albeit not significantly. The NBV-MB nonstructural protein μNS was involved in the induction of autophagy with viral infection.

conclusionsNBV-MB infection triggered autophagy. Also, the NBV nonstructural protein μNS may contribute to augmentation of autophagy upon viral infection.

Indexed as

AutophagyHost Microbial InteractionsVirus ReplicationCell LineHEK293 CellsHumansOrthoreovirusReoviridae InfectionsReverse GeneticsViral LoadViral ProteinsViral ProteinsAutophagyNelson BayOrthoreovirus replicationμNS

Identifiers

PMID31319897
PMCPMC6639940
OpenAlexW2960833775

What OpenQuestion holds

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Registered trials

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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.