Evidence map›Paper›PMID 26677217›Full record

ArticleThe Journal of biological chemistry2016

Modulation of Potassium Channels Inhibits Bunyavirus Infection.

Samantha Hover, Barnabas King, Bradley Hall, Eleni-Anna Loundras, Hussah Taqi, Janet Daly, Mark Dallas, Chris Peers, Esther Schnettler, Clive McKimmie and 3 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

39 citing papers in PubMed, 60 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

13 authors at 4 institutions in 1 country.

Samantha HoverFrom the School of Molecular and Cellular Biology, University of Leeds, Leeds LS2 9JT.
Barnabas KingSchool of Life Sciences, University of Nottingham, Nottingham NG7 2UH.
Bradley HallFrom the School of Molecular and Cellular Biology, University of Leeds, Leeds LS2 9JT.
Eleni-Anna LoundrasFrom the School of Molecular and Cellular Biology, University of Leeds, Leeds LS2 9JT.
Hussah TaqiFrom the School of Molecular and Cellular Biology, University of Leeds, Leeds LS2 9JT.
Janet DalyVeterinary Medicine and Science, University of Nottingham, Nottingham NG7 2RD.
Mark DallasSchool of Pharmacy, University of Reading, Reading RG6 6AP, and.
Chris PeersFrom the School of Molecular and Cellular Biology, University of Leeds, Leeds LS2 9JT.
Esther SchnettlerMRC-University of Glasgow Centre for Virus Research, Scotland, Glasgow G61 1QH, United Kingdom.
Clive McKimmieMRC-University of Glasgow Centre for Virus Research, Scotland, Glasgow G61 1QH, United Kingdom.
Alain KohlMRC-University of Glasgow Centre for Virus Research, Scotland, Glasgow G61 1QH, United Kingdom.
John N BarrFrom the School of Molecular and Cellular Biology, University of Leeds, Leeds LS2 9JT, J.N.Barr@leeds.ac.uk.
Jamel MankouriFrom the School of Molecular and Cellular Biology, University of Leeds, Leeds LS2 9JT, J.Mankouri@leeds.ac.uk.
University of Leeds · GBMRC University of Glasgow Centre for Virus Research · GBUniversity of Nottingham · GBUniversity of Reading · GB

Funding

Medical Research Council G1001724Medical Research Council MC_UU_12014/8
6 · The paper itself

Abstract

Bunyaviruses are considered to be emerging pathogens facilitated by the segmented nature of their genome that allows reassortment between different species to generate novel viruses with altered pathogenicity. Bunyaviruses are transmitted via a diverse range of arthropod vectors, as well as rodents, and have established a global disease range with massive importance in healthcare, animal welfare, and economics. There are no vaccines or anti-viral therapies available to treat human bunyavirus infections and so development of new anti-viral strategies is urgently required. Bunyamwera virus (BUNV; genus Orthobunyavirus) is the model bunyavirus, sharing aspects of its molecular and cellular biology with all Bunyaviridae family members. Here, we show for the first time that BUNV activates and requires cellular potassium (K(+)) channels to infect cells. Time of addition assays using K(+) channel modulating agents demonstrated that K(+) channel function is critical to events shortly after virus entry but prior to viral RNA synthesis/replication. A similar K(+) channel dependence was identified for other bunyaviruses namely Schmallenberg virus (Orthobunyavirus) as well as the more distantly related Hazara virus (Nairovirus). Using a rational pharmacological screening regimen, two-pore domain K(+) channels (K2P) were identified as the K(+) channel family mediating BUNV K(+) channel dependence. As several K2P channel modulators are currently in clinical use, our work suggests they may represent a new and safe drug class for the treatment of potentially lethal bunyavirus disease.

Indexed as

AedesAnimalsAntiviral AgentsBunyamwera virusBunyaviridae InfectionsCell LineChlorocebus aethiopsGene Expression Regulation, BacterialHost-Pathogen InteractionsHumansMesocricetusNairovirusOrthobunyavirusPotassium Channel BlockersPotassium Channels, Tandem Pore DomainVero CellsAntiviral AgentsKCNK1 protein, humanKCNK7 protein, humanKCNK9 protein, humanPotassium Channel Blockerspotassium channel protein TREK-1Potassium Channels, Tandem Pore Domainantiviral agention channelnegative-strand RNA viruspathogenesispotassium channel

Identifiers

PMID26677217
PMCPMC4751384
OpenAlexW2211940791

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.