ArticleJournal of virology1997
Two parvoviruses that cause different diseases in mink have different transcription patterns: transcription analysis of mink enteritis virus and Aleutian mink disease parvovirus in the same cell line.
Article in Journal of virology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 21 citations in OpenAlex.
- Loop-mediated Isothermal Amplification-Single Nucleotide Polymorphism Analysis for Detection and Differentiation of Wild-type and Vaccine Strains of Mink Enteritis Virus.Scientific reports · 2018Article
- CpG dinucleotide frequencies reveal the role of host methylation capabilities in parvovirus evolution.Journal of virology · 2013Article
- Internal polyadenylation of parvoviral precursor mRNA limits progeny virus production.Virology · 2012Article
- The capsid proteins of Aleutian mink disease virus activate caspases and are specifically cleaved during infection.Journal of virology · 2010Article
- The abundant R2 mRNA generated by aleutian mink disease parvovirus is tricistronic, encoding NS2, VP1, and VP2.Journal of virology · 2007Article
- The transcription profile of Aleutian mink disease virus in CRFK cells is generated by alternative processing of pre-mRNAs produced from a single promoter.Journal of virology · 2006Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The two parvoviruses of mink cause very different diseases. Mink enteritis virus (MEV) is associated with rapid, high-level viral replication and acute disease. In contrast, infection with Aleutian mink disease parvovirus (ADV) is associated with persistent, low-level viral replication and chronic severe immune dysregulation. In the present report, we have compared viral transcription in synchronized CRFK cells infected with either MEV or ADV using a nonradioactive RNase protection assay. The overall level of viral transcription was 20-fold higher in MEV- than in ADV-infected cells. Furthermore, MEV mRNA encoding structural proteins (MEV mRNA R3) was dominant throughout the infectious cycle, comprising approximately 80% of the total viral transcription products. In marked contrast, in ADV-infected cells, transcripts encoding nonstructural proteins (ADV mRNA R1 and R2) comprised more than 84% of the total transcripts at all times after infection, whereas ADV mRNA R3 comprised less than 16%. Thus, the ADV mRNA coding for structural proteins (ADV mRNA R3) was present at a level at least 100-fold lower than the corresponding MEV mRNA R3. These findings paralleled previous biochemical studies analyzing in vitro activities of the ADV and MEV promoters (J. Christensen, T. Storgaard, B. Viuff, B. Aasted, and S. Alexandersen, J. Virol. 67:1877-1886, 1993). The overall low levels of ADV mRNA and the paucity of the mRNA coding for ADV structural proteins may reflect an adaptation of the virus for low-level restricted infection.
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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.