ArticlePloS one2014
Feline calicivirus can tolerate gross changes of its minor capsid protein expression levels induced by changing translation reinitiation frequency or use of a separate VP2-coding mRNA.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 4 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.
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.
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Who cites it
4 citing papers in PubMed.
- Ribosomal control in RNA virus-infected cells.Frontiers in microbiology · 2022Review
- Major Capsid Protein Synthesis from the Genomic RNA of Feline Calicivirus.Journal of virology · 2020Article
- Please do not recycle! Translation reinitiation in microbes and higher eukaryotes.FEMS microbiology reviews · 2018Review
- Translational Control during Calicivirus Infection.Viruses · 2016Review
Corrections and comments
- Erratum issued
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Caliciviruses use reinitiation of translation governed by a 'termination upstream ribosomal binding site' (TURBS) for expression of their minor capsid protein VP2. Mutation analysis allowed to identify sequences surrounding the translational start/stop site of the feline calicivirus (FCV) that fine tune reinitiation frequency. A selection of these changes was introduced into the infectious FCV cDNA clone to check the influence of altered VP2 levels on virus replication. In addition, full length constructs were established that displayed a conformation, in which VP2 expression occurred under control of a duplicated subgenomic promoter. Viable viruses recovered from such constructs revealed a rather broad range of VP2 expression levels but comparable growth kinetics showing that caliciviruses can tolerate gross changes of the VP2 expression level.
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