Evidence map›Paper›PMID 39599533›Full record

ReviewPathogens (Basel, Switzerland)2024

Functional Role of Hepatitis C Virus NS5A in the Regulation of Autophagy.

Po-Yuan Ke, Chau-Ting Yeh

Abstract readReview
In one paragraph

Review in Pathogens (Basel, Switzerland), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. 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

2 authors.

Po-Yuan KeDepartment of Biochemistry and Molecular Biology, Graduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, Taoyuan 33302, Taiwan.ORCID 0000-0002-0471-0806
Chau-Ting YehLiver Research Center, Chang Gung Memorial Hospital, Taoyuan 33305, Taiwan.

Funding

Chang Gung Memorial Hospital CMRPD1M0671, CMRPD1N0221, CMRPD1N0431, CMRPD1P0261, and BMRPD01National Health Research Institute NHRI-EX103-10322SC, NHRI-EX104-10322SC, NHRI-EX105-10322SC and NHRI-EX106-10322SCNational Science and Technology Council MOST 109-2320-B-182-010-MY3 and NSTC 113-2311-B-182-001
6 · The paper itself

Abstract

Many types of RNA viruses, including the hepatitis C virus (HCV), activate autophagy in infected cells to promote viral growth and counteract the host defense response. Autophagy acts as a catabolic pathway in which unnecessary materials are removed via the lysosome, thus maintaining cellular homeostasis. The HCV non-structural 5A (NS5A) protein is a phosphoprotein required for viral RNA replication, virion assembly, and the determination of interferon (IFN) sensitivity. Recently, increasing evidence has shown that HCV NS5A can induce autophagy to promote mitochondrial turnover and the degradation of hepatocyte nuclear factor 1 alpha (HNF-1α) and diacylglycerol acyltransferase 1 (DGAT1). In this review, we summarize recent progress in understanding the detailed mechanism by which HCV NS5A triggers autophagy, and outline the physiological significance of the balance between host-virus interactions.

Indexed as

AutophagyHepacivirusHepatitis CViral Nonstructural ProteinsVirus ReplicationAnimalsHost-Pathogen InteractionsHumansRNA-Dependent RNA PolymeraseNS-5 protein, hepatitis C virusRNA-Dependent RNA PolymeraseViral Nonstructural Proteinsautophagychaperone-mediated autophagyHCVmicroautophagyselective autophagy

Identifiers

PMID39599533
PMCPMC11597459

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.