Evidence map›Paper›PMID 42412878›Full record

ArticlePLoS pathogens2026

The Bunyamwera orthobunyavirus Gc glycoprotein head and stalk drives an infectious virion assembly pathway specific for the insect host.

Amelia B Shaw, Hiu Nam Tse, Molly V Durawa, Owen Byford, Hayley M Pearson, Kenneth A Stapleford, Juan Fontana, John N Barr

Abstract read
In one paragraph

Article in PLoS pathogens, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Article
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.

Amelia B ShawSchool of Molecular and Cellular Biology, Faculty of Biological Sciences, University of Leeds, Leeds, United Kingdom.ORCID 0000-0002-6945-6124
Hiu Nam TseSchool of Molecular and Cellular Biology, Faculty of Biological Sciences, University of Leeds, Leeds, United Kingdom.
Molly V DurawaDepartment of Microbiology, New York University Grossman School of Medicine, New York, United States of America.
Owen ByfordSchool of Molecular and Cellular Biology, Faculty of Biological Sciences, University of Leeds, Leeds, United Kingdom.
Hayley M PearsonSchool of Molecular and Cellular Biology, Faculty of Biological Sciences, University of Leeds, Leeds, United Kingdom.
Kenneth A StaplefordDepartment of Microbiology, New York University Grossman School of Medicine, New York, United States of America.
Juan FontanaSchool of Molecular and Cellular Biology, Faculty of Biological Sciences, University of Leeds, Leeds, United Kingdom.
John N BarrSchool of Molecular and Cellular Biology, Faculty of Biological Sciences, University of Leeds, Leeds, United Kingdom.ORCID 0000-0002-9035-2039

Funding

Biotechnology and Biological Sciences Research Council BB/V007467/1Medical Research Council MR/T016159/1
6 · The paper itself

Abstract

The Orthobunyavirus genus of arthropod-borne segmented RNA viruses comprises important pathogens including the human-infecting Oropouche virus and ruminant-infecting Schmallenberg virus (SBV). The prototypical Bunyamwera orthobunyavirus (BUNV) possesses envelope-embedded glycoprotein Gn-Gc tripodal spikes, of which the ectodomains mediate virus entry, while endodomains interact with nucleoprotein (NP) enwrapped genome segments driving virion assembly. Interestingly, BUNV Gc head/stalk domains are redundant for virus growth in mammalian cells, consistent with isolations of SBV from ruminants bearing head/stalk deletions. However, these domains appear strictly maintained in orthobunyavirus isolations from arthropods in nature. To investigate the molecular mechanism that underlines this discrepancy, we compared the multiplication characteristics of wildtype BUNV (BUNV-WT) with a Gc head/stalk deleted BUNV (BUNV-∆7). In mammalian cells BUNV-WT and BUNV-∆7 grew to equivalent titres, whereas in insect cells BUNV-∆7 titres were 1000-fold lower and strikingly produced no virions following blood meal infection of Aedes mosquitoes. To understand this insect-specific restriction in virion production, we showed the intracellular abundance of BUNV-WT and BUNV-∆7 Gc and NP components were equivalent, suggesting the deletion impacted post-translational stages of the infection cycle. To explore this, we investigated Gc and ∆7-Gc interactions during BUNV-WT and BUNV-∆7 infections of both insect and mammalian cells by co-immunoprecipitation and multiplex mass spectrometry, revealing ∆7-Gc exhibited markedly reduced NP interactions in insect cells, potentially indicating reduced segment interactions during assembly. We hypothesize that the Gc head/stalk performs an insect cell-specific role in segment recruitment during virion formation, and that maintenance in nature of full-length Gc is due to this essential role in the insect host.

Indexed as

Bunyamwera virusBunyaviridae InfectionsGlycoproteinsViral Envelope ProteinsVirus AssemblyAnimalsHumansVirionGlycoproteinsViral Envelope Proteins

Identifiers

PMID42412878
PMCPMC13399505

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Registered trials

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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.