Evidence map›Paper›PMID 30544615›Full record

ReviewInternational journal of molecular sciences2018

The Multifaceted Roles of Autophagy in Flavivirus-Host Interactions.

Po-Yuan Ke

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
7.4field-weighted citation impact, top 3% 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

40 citing papers in PubMed, 72 citations in OpenAlex.

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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

1 author at 1 institution in 1 country.

Po-Yuan KeDepartment of Biochemistry & Molecular Biology and Graduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, Taoyuan 33302, Taiwan. pyke0324@mail.cgu.edu.tw.ORCID 0000-0002-0471-0806
Chang Gung University · TW

Funding

Ministry of Science and Technology, National Health Research Institute, and Chang Gung Memorial Hospital, Taiwan, Republic of China MOST 102-2320-B-182-037-MY3, MOST 105-2628-B-182-001-MY3, NHRI-EX103-10322SC, NHRI-EX104-10322SC, NHRI-EX105-10322SC, NHRI-EX106-10322SC, CMRPD1C0211, CMRPD1D0021, CMRPD1D0022, CMRPD1D0023, CMRPD1G0281, CRRPD1F0031, and CMRPG3F0571
6 · The paper itself

Abstract

Autophagy is an evolutionarily conserved cellular process in which intracellular components are eliminated via lysosomal degradation to supply nutrients for organelle biogenesis and metabolic homeostasis. Flavivirus infections underlie multiple human diseases and thus exert an immense burden on public health worldwide. Mounting evidence indicates that host autophagy is subverted to modulate the life cycles of flaviviruses, such as hepatitis C virus, dengue virus, Japanese encephalitis virus, West Nile virus and Zika virus. The diverse interplay between autophagy and flavivirus infection not only regulates viral growth in host cells but also counteracts host stress responses induced by viral infection. In this review, we summarize the current knowledge on the role of autophagy in the flavivirus life cycle. We also discuss the impacts of virus-induced autophagy on the pathogeneses of flavivirus-associated diseases and the potential use of autophagy as a therapeutic target for curing flavivirus infections and related human diseases.

Indexed as

AnimalsAutophagyDengue VirusEncephalitis Virus, JapaneseFlavivirusHepacivirusHost-Pathogen InteractionsHumansZika VirusAutophagyDengue virusFlaviviridaeHepatitis C virusJapanese encephalitis virusselective autophagyWest Nile virusZika virus

Identifiers

PMID30544615
PMCPMC6321027
OpenAlexW2904197983

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.