Evidence map›Paper›PMID 30456659›Full record

ArticleVirologica Sinica2019

MicroRNA-135a Modulates Hepatitis C Virus Genome Replication through Downregulation of Host Antiviral Factors.

Catherine Sodroski, Brianna Lowey, Laura Hertz, T Jake Liang, Qisheng Li

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

Article in Virologica Sinica, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.0field-weighted citation impact, top 29% 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

19 citing papers in PubMed, 23 citations in OpenAlex.

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  18. The Role of Non-coding RNAs in Viral Myocarditis.Frontiers in cellular and infection microbiology · 2020
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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

5 authors at 1 institution in 1 country.

Catherine SodroskiLiver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, 20892, USA.
Brianna LoweyLiver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, 20892, USA.
Laura HertzLiver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, 20892, USA.
T Jake LiangLiver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, 20892, USA. jakel@bdg10.niddk.nih.gov.ORCID http://orcid.org/0000-0003-3828-702X
Qisheng LiLiver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, 20892, USA. liqisheng@niddk.nih.gov.ORCID http://orcid.org/0000-0002-4181-1972
National Institutes of Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cellular microRNAs (miRNAs) have been shown to modulate HCV infection via directly acting on the viral genome or indirectly through targeting the virus-associated host factors. Recently we generated a comprehensive map of HCV-miRNA interactions through genome-wide miRNA functional screens and transcriptomics analyses. Many previously unappreciated cellular miRNAs were identified to be involved in HCV infection, including miR-135a, a human cancer-related miRNA. In the present study, we investigated the role of miR-135a in regulating HCV life cycle and showed that it preferentially enhances viral genome replication. Bioinformatics-based integrative analyses and subsequent functional assays revealed three antiviral host factors, including receptor interacting serine/threonine kinase 2 (RIPK2), myeloid differentiation primary response 88 (MYD88), and C-X-C motif chemokine ligand 12 (CXCL12), as bona fide targets of miR-135a. These genes have been shown to inhibit HCV infection at the RNA replication stage. Our data demonstrated that repression of key host restriction factors mediated the proviral effect of miR-135a on HCV propagation. In addition, miR-135a hepatic abundance is upregulated by HCV infection in both cultured hepatocytes and human liver, likely mediating a more favorable environment for viral replication and possibly contributing to HCV-induced liver malignancy. These results provide novel insights into HCV-host interactions and unveil molecular pathways linking miRNA biology to HCV pathogenesis.

Indexed as

Genome, ViralVirus ReplicationChemokine CXCL12Down-RegulationHepacivirusHepatitis CHepatocytesHost-Pathogen InteractionsHumansLiverLiver NeoplasmsMicroRNAsMyeloid Differentiation Factor 88Receptor-Interacting Protein Serine-Threonine Kinase 2Transcriptional ActivationChemokine CXCL12CXCL12 protein, humanMicroRNAsMIRN135 microRNA, humanMYD88 protein, humanMyeloid Differentiation Factor 88Receptor-Interacting Protein Serine-Threonine Kinase 2RIPK2 protein, humanAntiviral factorsGenome replicationHepatitis C virus (HCV)miR-135aVirus–host interactions

Identifiers

PMID30456659
PMCPMC6513812
OpenAlexW2900836341

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.