ArticleJournal of virology2005
The Bunyamwera virus mRNA transcription signal resides within both the 3' and the 5' terminal regions and allows ambisense transcription from a model RNA segment.
Article in Journal of virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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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
18 citing papers in PubMed, 31 citations in OpenAlex.
- The bipartite promoter ofJournal of virology · 2023Article
- Segmented, Negative-Sense RNA Viruses of Humans: Genetic Systems and Experimental Uses of Reporter Strains.Annual review of virology · 2023Review
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- A comprehensive list of the Bunyavirales replication promoters reveals a unique promoter structure in Nairoviridae differing from other virus families.Scientific reports · 2022Article
- Article
- Mutagenic Analysis of Hazara Nairovirus Nontranslated Regions during Single- and Multistep Growth Identifies both Attenuating and Functionally Critical Sequences for Virus Replication.Journal of virology · 2020Article
- Article
- Structural and functional similarities in bunyaviruses: Perspectives for pan-bunya antivirals.Reviews in medical virology · 2019Review
- Generation of a Recombinant Akabane Virus Expressing Enhanced Green Fluorescent Protein.Journal of virology · 2015Article
- Flexibility of bunyavirus genomes: creation of an orthobunyavirus with an ambisense S segment.Journal of virology · 2015Article
- Systems to establish bunyavirus genome replication in the absence of transcription.Journal of virology · 2013Article
- Minigenomes, transcription and replication competent virus-like particles and beyond: reverse genetics systems for filoviruses and other negative stranded hemorrhagic fever viruses.Antiviral research · 2011Review
- Amino acid changes within the Bunyamwera virus nucleocapsid protein differentially affect the mRNA transcription and RNA replication activities of assembled ribonucleoprotein templates.The Journal of general virology · 2011Article
- Bunyamwera virus can repair both insertions and deletions during RNA replication.RNA (New York, N.Y.) · 2010Article
- Reverse genetics technology for Rift Valley fever virus: current and future applications for the development of therapeutics and vaccines.Antiviral research · 2009Review
- Investigating the specificity and stoichiometry of RNA binding by the nucleocapsid protein of Bunyamwera virus.RNA (New York, N.Y.) · 2009Article
- Characterization of Rift Valley fever virus transcriptional terminations.Journal of virology · 2007Article
- Mutational analysis of the lassa virus promoter.Journal of virology · 2006Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Bunyamwera virus (BUNV) is the prototype of the Bunyaviridae family of RNA viruses. BUNV genomic strands are templates for both replication and transcription, whereas the antigenomic RNAs serve only as templates for replication. By mutagenesis of model templates, we showed that the BUNV transcription promoter comprises elements within both the 3' and the 5' nontranslated regions. Using this information, we designed a model ambisense BUNV segment that transcribed BUNV S mRNA from the genomic strand and green fluorescent protein (GFP) mRNA from the antigenome. Demonstration of GFP expression showed that this ambisense strategy represents a viable approach for generating BUNV segments able to express additional proteins.
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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.