Evidence map›Paper›PMID 23633945›Full record

ArticlePLoS pathogens2013

HCV-induced miR-21 contributes to evasion of host immune system by targeting MyD88 and IRAK1.

Yanni Chen, Junbo Chen, Hui Wang, Jingjing Shi, Kailang Wu, Shi Liu, Yingle Liu, Jianguo Wu

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PLoS pathogens, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 144 papers.

0numbers the graph read from it
0cells of the map it votes in
144citing papers in PubMed
10.4field-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

144 citing papers in PubMed, 237 citations in OpenAlex.

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84 more citing papers are in PubMed but not listed here.

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

8 authors at 4 institutions in 1 country.

Yanni ChenState Key Laboratory of Virology, College of Life Sciences, and Chinese-French Liver Disease Research Institute at Zhongnan Hospital, Wuhan University, Wuhan, Hubei, PR China.
Junbo Chen
Hui Wang
Jingjing Shi
Kailang Wu
Shi Liu
Yingle Liu
Jianguo Wu
Zhongnan Hospital of Wuhan University · CNWuhan University · CNChinese Academy of Sciences · CNWuhan Institute of Bioengineering · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Upon recognition of viral components by pattern recognition receptors, such as the toll-like receptors (TLRs) and retinoic acid-inducible gene I (RIG-I)-like helicases, cells are activated to produce type I interferon (IFN) and proinflammatory cytokines. These pathways are tightly regulated by the host to prevent an inappropriate cellular response, but viruses can modulate these pathways to proliferate and spread. In this study, we revealed a novel mechanism in which hepatitis C virus (HCV) evades the immune surveillance system to proliferate by activating microRNA-21 (miR-21). We demonstrated that HCV infection upregulates miR-21, which in turn suppresses HCV-triggered type I IFN production, thus promoting HCV replication. Furthermore, we demonstrated that miR-21 targets two important factors in the TLR signaling pathway, myeloid differentiation factor 88 (MyD88) and interleukin-1 receptor-associated kinase 1 (IRAK1), which are involved in HCV-induced type I IFN production. HCV-mediated activation of miR-21 expression requires viral proteins and several signaling components. Moreover, we identified a transcription factor, activating protein-1 (AP-1), which is partly responsible for miR-21 induction in response to HCV infection through PKCε/JNK/c-Jun and PKCα/ERK/c-Fos cascades. Taken together, our results indicate that miR-21 is upregulated during HCV infection and negatively regulates IFN-α signaling through MyD88 and IRAK1 and may be a potential therapeutic target for antiviral intervention.

Indexed as

Immune EvasionAdaptor Proteins, Vesicular TransportCell Line, TumorDEAD-box RNA HelicasesExtracellular Signal-Regulated MAP KinasesHEK293 CellsHepacivirusHepatitis CHumansInterferon-alphaInterferon Regulatory Factor-3Interleukin-1 Receptor-Associated KinasesJNK Mitogen-Activated Protein KinasesMAP Kinase Signaling SystemMicroRNAsMyeloid Differentiation Factor 88Adaptor Proteins, Vesicular TransportDEAD-box RNA HelicasesExtracellular Signal-Regulated MAP KinasesInterferon-alphaInterferon Regulatory Factor-3Interleukin-1 Receptor-Associated KinasesIRAK1 protein, humanIRF3 protein, humanJNK Mitogen-Activated Protein KinasesMicroRNAsMIRN21 microRNA, humanMYD88 protein, humanMyeloid Differentiation Factor 88NS3 protein, flavivirusNS4A protein, flavivirusNS5 protein, flavivirusNucleoside-TriphosphataseProtein Kinase CProto-Oncogene Proteins c-fosRNA HelicasesRNA, Small InterferingSerine EndopeptidasesTICAM1 protein, humanTLR7 protein, humanToll-Like Receptor 7Viral Nonstructural ProteinsViral Proteases

Identifiers

PMID23633945
PMCPMC3635988
OpenAlexW2009663348

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.