Evidence map›Paper›PMID 28404855›Full record

ArticleJournal of virology2017

Genome-Wide Screening Uncovers the Significance of N-Sulfation of Heparan Sulfate as a Host Cell Factor for Chikungunya Virus Infection.

Atsushi Tanaka, Uranan Tumkosit, Shota Nakamura, Daisuke Motooka, Natsuko Kishishita, Thongkoon Priengprom, Areerat Sa-Ngasang, Taroh Kinoshita, Naokazu Takeda, Yusuke Maeda

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
9.4field-weighted citation impact, top 2% 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

70 citing papers in PubMed, 103 citations in OpenAlex.

  1. Article
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  3. CRISPR-Cas9 screening revealsMolecular therapy. Advances · 2026
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  5. The SMARCA4-TMEM47 axis plays an essential role in chikungunya virus RNA replication.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
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10 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

10 authors at 3 institutions in 2 countries.

Atsushi TanakaResearch Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan.
Uranan TumkositThailand-Japan Research Collaboration Center on Emerging and Re-emerging Infections, Department of Medical Sciences, Ministry of Public Health, Nonthaburi, Thailand.
Shota NakamuraResearch Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan.
Daisuke MotookaResearch Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan.
Natsuko KishishitaResearch Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan.
Thongkoon PriengpromThailand-Japan Research Collaboration Center on Emerging and Re-emerging Infections, Department of Medical Sciences, Ministry of Public Health, Nonthaburi, Thailand.
Areerat Sa-NgasangArbovirus Section, National Institute of Health, Department of Medical Sciences, Ministry of Public Health, Nonthaburi, Thailand.
Taroh KinoshitaResearch Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan.
Naokazu TakedaResearch Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan.
Yusuke MaedaResearch Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan ymaeda@biken.osaka-u.ac.jp.
Ministry of Public Health · THOsaka University · JPDepartment of Medical Sciences · TH

Funding

Wellcome Trust
6 · The paper itself

Abstract

The molecular mechanisms underlying chikungunya virus (CHIKV) infection are poorly characterized. In this study, we analyzed the host factors involved in CHIKV infection using genome-wide screening. Human haploid HAP1 cells, into which an exon-trapping vector was introduced, were challenged with a vesicular stomatitis virus pseudotype bearing the CHIKV E3 to E1 envelope proteins. Analysis of genes enriched in the cells resistant to the pseudotyped virus infection unveiled a critical role of N-sulfation of heparan sulfate (HS) for the infectivity of the clinically isolated CHIKV Thai#16856 strain to HAP1 cells. Knockout of NDST1 that catalyzes N-sulfation of HS greatly decreased the binding and infectivity of CHIKV Thai#16856 strain but not infectivity of Japanese encephalitis virus (JEV) and yellow fever virus (YFV). While glycosaminoglycans were commonly required for the efficient infectivity of CHIKV, JEV, and YFV, as shown by using

Indexed as

Virus AttachmentCell LineChikungunya virusEncephalitis Virus, JapaneseGene Knockout TechniquesGenetic TestingGlucuronosyltransferaseHeparan SulfateHumansMembrane ProteinsSulfotransferasesYellow fever virusB3GAT3 protein, humanGlucuronosyltransferaseHeparan Sulfateheparitin sulfotransferaseMembrane ProteinsSulfotransferasesTM9SF2 protein, humanchikungunyaglycosaminoglycanheparan sulfateTM9SF2

Identifiers

PMID28404855
PMCPMC5469253
OpenAlexW2607190021

What OpenQuestion holds

Textmetadata
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.