Evidence map›Paper›PMID 33059318›Full record

ArticleVirology2021

Host gene expression modulated by Zika virus infection of human-293 cells.

Sachi Horibata, Tadahisa Teramoto, Navin Vijayarangan, Skyler Kuhn, Raji Padmanabhan, Sona Vasudevan, Michael Gottesman, Radhakrishnan Padmanabhan

Open access · greenAbstract read
In one paragraph

Article in Virology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.9field-weighted citation impact, top 22% 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

5 citing papers in PubMed, 11 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

8 authors at 2 institutions in 1 country.

Sachi HoribataLaboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, United States.
Tadahisa TeramotoDepartment of Microbiology and Immunology, Georgetown University Medical Center, Washington DC, United States.
Navin VijayaranganDepartment of Biochemistry, Molecular and Cell Biology, Georgetown University Medical Center, Washington D.C, 20057, United States.
Skyler KuhnCCR Collaborative Bioinformatics Resource, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, United States.
Raji PadmanabhanLaboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, United States.
Sona VasudevanDepartment of Biochemistry, Molecular and Cell Biology, Georgetown University Medical Center, Washington D.C, 20057, United States.
Michael GottesmanLaboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, United States.
Radhakrishnan PadmanabhanDepartment of Microbiology and Immunology, Georgetown University Medical Center, Washington DC, United States. Electronic address: rp55@georgetown.edu.
National Institutes of Health · USGeorgetown University · US

Funding

Mechanisms of non-classical multidrug resistance in cancerZIABC010830 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI GOTTESMAN, MICHAEL · 2009 to 2025
$19.6M
Intramural NIH HHS ZIA BC010830
6 · The paper itself

Abstract

The HEK-293 cell line was created in 1977 by transformation of primary human embryonic kidney cells with sheared adenovirus type 5 DNA. A previous study determined that the HEK-293 cells have neuronal markers rather than kidney markers. In this study, we tested the hypothesis whether Zika virus (ZIKV), a neurotropic virus, is able to infect and replicate in the HEK-293 cells. We show that the HEK-293 cells infected with ZIKV support viral replication as shown by indirect immunofluorescence (IFA) and quantitative reverse transcriptase-PCR (qRT-PCR). We performed RNA-seq analysis on the ZIKV-infected and the control uninfected HEK-293 cells and find 659 genes that are differentially transcribed in ZIKV-infected HEK-293 cells as compared to uninfected cells. The results show that the top 10 differentially transcribed and upregulated genes are involved in antiviral and inflammatory responses. Seven upregulated genes, IFNL1, DDX58, CXCL10, ISG15, KCNJ15, IFNIH1, and IFIT2, were validated by qRT-PCR. Altogether, our findings show that ZIKV infection alters host gene expression by affecting their antiviral and inflammatory responses.

Indexed as

Gene Expression RegulationApoptosis Regulatory ProteinsChemokine CXCL10CytokinesDEAD Box Protein 58Fluorescent Antibody Technique, IndirectHEK293 CellsHost Microbial InteractionsHumansInflammationInterferon-Induced Helicase, IFIH1Interferon LambdaInterferonsInterleukinsPotassium Channels, Inwardly RectifyingReceptors, ImmunologicApoptosis Regulatory ProteinsChemokine CXCL10CytokinesDEAD Box Protein 58IFIH1 protein, humanIFIT2 protein, humanInterferon-Induced Helicase, IFIH1Interferon Lambdainterferon-lambda, humanInterferonsInterleukinsISG15 protein, humanKCNJ15 protein, humanPotassium Channels, Inwardly RectifyingReceptors, ImmunologicRIGI protein, humanRNA-Binding ProteinsUbiquitinsAnalysis of host gene expression by RNA-seqDerived from transformation by human adenovirus oncogenesHEK-293 cells with neuronal markers as a host for neurotropic Zika virusHuman embryonic kidney (HEK-293) cells

Identifiers

PMID33059318
PMCPMC8383823
OpenAlexW3092567145

What OpenQuestion holds

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LicenceTDM
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.