ArticlePloS one2014
Genome sequence analysis of in vitro and in vivo phenotypes of Bunyamwera and Ngari virus isolates from northern Kenya.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Preliminary evidence that Bunyamwera virus causes severe disease characterized by systemic vascular and multiorgan necrosis in an immunocompromised mouse model.The Journal of general virology · 2024Article
- Immunocompetent hamsters as a model for orthobunyavirus-induced neuroinvasion and neuropathology.PLoS neglected tropical diseases · 2023Article
- Urban risk factors for human Rift Valley fever virus exposure in Kenya.PLOS global public health · 2022Article
- Comparative characterization of the reassortant Orthobunyavirus Ngari with putative parental viruses, Bunyamwera and Batai:The Journal of general virology · 2021Article
- Identification of Bunyamwera and Possible OtherThe American journal of tropical medicine and hygiene · 2020Article
- Structural and functional similarities in bunyaviruses: Perspectives for pan-bunya antivirals.Reviews in medical virology · 2019Review
- Aedes vittatus in Spain: current distribution, barcoding characterization and potential role as a vector of human diseases.Parasites & vectors · 2018Article
- A Review of Bunyamwera, Batai, and Ngari Viruses: UnderstudiedFrontiers in veterinary science · 2018Review
- Genetic divergence of Chikungunya virus plaque variants from the Comoros Island (2005).Virus genes · 2015Article
- Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Biological phenotypes of tri-segmented arboviruses display characteristics that map to mutation/s in the S, M or L segments of the genome. Plaque variants have been characterized for other viruses displaying varied phenotypes including attenuation in growth and/or pathogenesis. In order to characterize variants of Bunyamwera and Ngari viruses, we isolated individual plaque size variants; small plaque (SP) and large plaque (LP) and determined in vitro growth properties and in vivo pathogenesis in suckling mice. We performed gene sequencing to identify mutations that may be responsible for the observed phenotype. The LP generally replicated faster than the SP and the difference in growth rate was more pronounced in Bunyamwera virus isolates. Ngari virus isolates were more conserved with few point mutations compared to Bunyamwera virus isolates which displayed mutations in all three genome segments but majority were silent mutations. Contrary to expectation, the SP of Bunyamwera virus killed suckling mice significantly earlier than the LP. The LP attenuation may probably be due to a non-synonymous substitution (T858I) that mapped within the active site of the L protein. In this study, we identify natural mutations whose exact role in growth and pathogenesis need to be determined through site directed mutagenesis studies.
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