ArticlePLoS pathogens2018
Bunyavirus requirement for endosomal K+ reveals new roles of cellular ion channels during infection.
Article in PLoS pathogens, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
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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.
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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.
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Who cites it
37 citing papers in PubMed, 52 citations in OpenAlex.
- Oropouche virus infection: clinical spectrum, geographic expansion, and emerging maternal-fetal implications.Infection · 2026Review
- The Bunyamwera orthobunyavirus Gc glycoprotein head and stalk drives an infectious virion assembly pathway specific for the insect host.PLoS pathogens · 2026Article
- A Potent Inhibitor of Human Cytomegalovirus Infection Works Post-Entry Specifically in Differentiating Myelo-Monocytic Cells.Pathogens (Basel, Switzerland) · 2026Article
- Identification of cellular ion channels that facilitate Hazara nairovirus infection enables selection of clinically approved compounds with anti-nairoviral properties.Scientific reports · 2026Article
- Targeting virus-interacting host ion channels as a novel antiviral strategy.Acta pharmacologica Sinica · 2026Review
- Review
- The Role of Orthobunyavirus Glycoprotein Gc in the Viral Life Cycle: From Viral Entry to Egress.Molecules (Basel, Switzerland) · 2025Review
- The plant rhabdovirus viroporin P9 facilitates insect-mediated virus transmission in barley.The Plant cell · 2024Article
- KCNE4 is a crucial host factor for Orf virus infection by mediating viral entry.Virology journal · 2024Article
- Article
- Article
- Organisation of the orthobunyavirus tripodal spike and the structural changes induced by low pH and KNature communications · 2023Article
- IFN-stimulated metabolite transporter ENT3 facilitates viral genome release.EMBO reports · 2023Article
- High Levels of Extracellular Potassium Can Delay Myxoma Virus Replication by Preventing Release of Virions from the Endosomes.Journal of virology · 2023Article
- The Orthobunyavirus Germiston Enters Host Cells from Late Endosomes.Journal of virology · 2022Article
- Structural Modifications and Biological Evaluations of Rift Valley Fever Virus Inhibitors Identified from Chemical Library Screening.ACS omega · 2022Article
- Chemical Evolution of Rhinovirus Identifies Capsid-Destabilizing Mutations Driving Low-pH-Independent Genome Uncoating.Journal of virology · 2022Article
- TrkA serves as a virulence modulator inFrontiers in cellular and infection microbiology · 2022Article
- COVID-19: the CaMKII-like system of S protein drives membrane fusion and induces syncytial multinucleated giant cells.Immunologic research · 2021Article
- Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
In order to multiply and cause disease a virus must transport its genome from outside the cell into the cytosol, most commonly achieved through the endocytic network. Endosomes transport virus particles to specific cellular destinations and viruses exploit the changing environment of maturing endocytic vesicles as triggers to mediate genome release. Previously we demonstrated that several bunyaviruses, which comprise the largest family of negative sense RNA viruses, require the activity of cellular potassium (K+) channels to cause productive infection. Specifically, we demonstrated a surprising role for K+ channels during virus endosomal trafficking. In this study, we have used the prototype bunyavirus, Bunyamwera virus (BUNV), as a tool to understand why K+ channels are required for progression of these viruses through the endocytic network. We report three major findings: First, the production of a dual fluorescently labelled bunyavirus to visualize virus trafficking in live cells. Second, we show that BUNV traffics through endosomes containing high [K+] and that these K+ ions influence the infectivity of virions. Third, we show that K+ channel inhibition can alter the distribution of K+ across the endosomal system and arrest virus trafficking in endosomes. These data suggest high endosomal [K+] is a critical cue that is required for virus infection, and is controlled by cellular K+ channels resident within the endosome network. This highlights cellular K+ channels as druggable targets to impede virus entry, infection and disease.
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Registered trials
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.