ArticleJournal of virology2003
Complementation of a deletion in the rubella virus p150 nonstructural protein by the viral capsid protein.
Article in Journal of virology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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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
27 citing papers in PubMed, 40 citations in OpenAlex.
- A self-amplifying RNA vector based on rubella virus for mRNA therapeutics and vaccine applications.Molecular therapy. Nucleic acids · 2026Article
- Exogenous Rubella Virus Capsid Proteins Enhance Virus Genome Replication.Pathogens (Basel, Switzerland) · 2022Article
- Short self-interacting N-terminal region of rubella virus capsid protein is essential for cooperative actions of capsid and nonstructural p150 proteins.Journal of virology · 2014Article
- Review
- Live attenuated rubella vectors expressing SIV and HIV vaccine antigens replicate and elicit durable immune responses in rhesus macaques.Retrovirology · 2013Article
- Live attenuated rubella viral vectors stably express HIV and SIV vaccine antigens while reaching high titers.Vaccine · 2012Article
- Determinants in the maturation of rubella virus p200 replicase polyprotein precursor.Journal of virology · 2012Article
- Binding of cellular p32 protein to the rubella virus P150 replicase protein via PxxPxR motifs.The Journal of general virology · 2012Article
- Rubella virus-like replicon particles: analysis of encapsidation determinants and non-structural roles of capsid protein in early post-entry replication.The Journal of general virology · 2012Article
- The Rubella virus capsid is an anti-apoptotic protein that attenuates the pore-forming ability of Bax.PLoS pathogens · 2011Article
- Calcium-dependent association of calmodulin with the rubella virus nonstructural protease domain.The Journal of biological chemistry · 2010Article
- The rubella virus capsid protein inhibits mitochondrial import.Journal of virology · 2010Article
- Functional replacement of a domain in the rubella virus p150 replicase protein by the virus capsid protein.Journal of virology · 2009Article
- Deletions of the hypervariable region (HVR) in open reading frame 1 of hepatitis E virus do not abolish virus infectivity: evidence for attenuation of HVR deletion mutants in vivo.Journal of virology · 2009Article
- Bioinformatic and physical characterizations of genome-scale ordered RNA structure in mammalian RNA viruses.Journal of virology · 2008Article
- Rubella virus capsid protein interacts with poly(a)-binding protein and inhibits translation.Journal of virology · 2008Article
- Analysis of the selective advantage conferred by a C-E1 fusion protein synthesized by rubella virus DI RNAs.Virology · 2007Article
- Identification of a Ca2+-binding domain in the rubella virus nonstructural protease.Journal of virology · 2007Article
- Novel replication complex architecture in rubella replicon-transfected cells.Cellular microbiology · 2007Article
- Analyses of phosphorylation events in the rubella virus capsid protein: role in early replication events.Journal of virology · 2006Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Rubella virus (RUB) replicons with an in-frame deletion of 507 nucleotides between two NotI sites in the P150 nonstructural protein (DeltaNotI) do not replicate (as detected by expression of a reporter gene encoded by the replicon) but can be amplified by wild-type helper virus (Tzeng et al., Virology 289:63-73, 2001). Surprisingly, virus with DeltaNotI was viable, and it was hypothesized that this was due to complementation of the NotI deletion by one of the virion structural protein genes. Introduction of the capsid (C) protein gene into DeltaNotI-containing replicons as an in-frame fusion with a reporter gene or cotransfection with both DeltaNotI replicons and RUB replicon or plasmid constructs containing the C gene resulted in replication of the DeltaNotI replicon, confirming the hypothesis that the C gene was the structural protein gene responsible for complementation and demonstrating that complementation could occur either in cis or in trans. Approximately the 5' one-third of the C gene was necessary for complementation. Mutations that prevented translation of the C protein while minimally disturbing the C gene sequence abrogated complementation, while synonymous codon mutations that changed the C gene sequence without affecting the amino acid sequence at the 5' end of the C gene had no effect on complementation, indicating that the C protein, not the C gene RNA, was the moiety responsible for complementation. Complementation occurred at a basic step in the virus replication cycle, because DeltaNotI replicons failed to accumulate detectable virus-specific RNA.
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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.