ArticleJournal of virology2018
The 5' Untranslated Region of the Capsid Protein 2 Gene of Mink Enteritis Virus Is Essential for Its Expression.
Article in Journal of virology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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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Who cites it
2 citing papers in PubMed, 10 citations in OpenAlex.
- Multiplex one-step RT‒qPCR assays for simultaneous detection of AMDV, MEV and CDV.BMC veterinary research · 2025Article
- Two Short Repeats in the 5' Untranslated Region of Insulin-like Androgenic Gland Factor inInternational journal of molecular sciences · 2022Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mink enteritis virus (MEV), as a parvovirus, is among the smallest of the animal DNA viruses. The limited genome leads to multifunctional sequences and complex gene expression regulation. Here, we show that the expression of viral capsid protein 2 (VP2) of MEV requires its 5' untranslated regions (5' UTR) which promote VP2 gene expression at both transcriptional and translational levels. The expression of VP2 was inhibited in several common eukaryotic expression vectors. Our data showed that the 5' UTR of VP2 enhanced capsid gene transcription but not increased stability or promotes nucleocytoplasmic export of VP2 mRNA. Analysis of the functions of 5' UTR fragments showed that the proximal region (nucleotides [nt] 1 to 270; that is, positions +1 to +270 relative to the transcription initiation site, nt 2048 to 2317 of MEV-L) of 5' UTR of VP2 was necessary for VP2 transcription and also promoted the activity of P38 promoter. Unexpectedly, further analysis showed that deletion of the distal region (nt 271 to 653) of the 5' UTR of VP2 almost completely abolished VP2 translation in the presence of P38, whereas the transcription was still induced significantly. Furthermore, using a luciferase reporter bicistronic system, we identified that the 5' UTR had an internal ribosome entry site-like function which could be enhanced by NS1 via the site at nt 382 to 447. Mutation of the 5' UTR in the MEV full-length clones further showed that the 5' UTR was required for VP2 gene expression. Together, our data reveal an undiscovered function of 5' UTR of MEV VP2 in regulating viral gene expression.
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