ArticleJournal of virology2007
Signal peptide and helical bundle domains of virulent canine distemper virus fusion protein restrict fusogenicity.
Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 36 citations in OpenAlex.
- Completion of the Genome Sequence of a Historic CDV Vaccine Strain, Rockborn: Evolutionary and Epidemiologic Implications.Veterinary sciences · 2026Article
- Fusion protein and hemagglutinin of canine distemper virus co-induce apoptosis in canine mammary tumor cells.Journal of cancer research and clinical oncology · 2023Article
- A highly virulent canine distemper virus strain isolated from vaccinated mink in China.Virus genes · 2021Article
- Development of a double monoclonal antibody-based sandwich enzyme-linked immunosorbent assay for detecting canine distemper virus.Applied microbiology and biotechnology · 2020Article
- Structures of the prefusion form of measles virus fusion protein in complex with inhibitors.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Canine Distemper Virus Fusion Activation: Critical Role of Residue E123 of CD150/SLAM.Journal of virology · 2016Article
- Article
- Hairless Streaks in Cattle Implicate TSR2 in Early Hair Follicle Formation.PLoS genetics · 2015Article
- Sequential conformational changes in the morbillivirus attachment protein initiate the membrane fusion process.PLoS pathogens · 2015Article
- Structure and antigenicity analysis of the IgG gene for Nyctereutes procyonoides.Central-European journal of immunology · 2015Article
- Molecular determinants defining the triggering range of prefusion F complexes of canine distemper virus.Journal of virology · 2014Article
- Article
- Deduced sequences of the membrane fusion and attachment proteins of canine distemper viruses isolated from dogs and wild animals in Korea.Virus genes · 2013Article
- Mechanism for active membrane fusion triggering by morbillivirus attachment protein.Journal of virology · 2013Article
- Structural rearrangements of the central region of the morbillivirus attachment protein stalk domain trigger F protein refolding for membrane fusion.The Journal of biological chemistry · 2012Article
- Morbillivirus glycoprotein expression induces ER stress, alters Ca2+ homeostasis and results in the release of vasostatin.PloS one · 2012Article
- Canine distemper virus infects canine keratinocytes and immune cells by using overlapping and distinct regions located on one side of the attachment protein.Journal of virology · 2011Article
- Identification of key residues in virulent canine distemper virus hemagglutinin that control CD150/SLAM-binding activity.Journal of virology · 2010Article
- Two domains of the V protein of virulent canine distemper virus selectively inhibit STAT1 and STAT2 nuclear import.Journal of virology · 2010Article
- The Asia 2 specific signal peptide region and other domains in fusion protein genes characterized Asia 1 and Asia 2 canine distemper viruses.Virology journal · 2009Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Persistence in canine distemper virus (CDV) infection is correlated with very limited cell-cell fusion and lack of cytolysis induced by the neurovirulent A75/17-CDV compared to that of the cytolytic Onderstepoort vaccine strain. We have previously shown that this difference was at least in part due to the amino acid sequence of the fusion (F) protein (P. Plattet, J. P. Rivals, B. Zuber, J. M. Brunner, A. Zurbriggen, and R. Wittek, Virology 337:312-326, 2005). Here, we investigated the molecular mechanisms of the neurovirulent CDV F protein underlying limited membrane fusion activity. By exchanging the signal peptide between both F CDV strains or replacing it with an exogenous signal peptide, we demonstrated that this domain controlled intracellular and consequently cell surface protein expression, thus indirectly modulating fusogenicity. In addition, by serially passaging a poorly fusogenic virus and selecting a syncytium-forming variant, we identified the mutation L372W as being responsible for this change of phenotype. Intriguingly, residue L372 potentially is located in the helical bundle domain of the F(1) subunit. We showed that this mutation drastically increased fusion activity of F proteins of both CDV strains in a signal peptide-independent manner. Due to its unique structure even among morbilliviruses, our findings with respect to the signal peptide are likely to be specifically relevant to CDV, whereas the results related to the helical bundle add new insights to our growing understanding of this class of F proteins. We conclude that different mechanisms involving multiple domains of the neurovirulent A75/17-CDV F protein act in concert to limit fusion activity, preventing lysis of infected cells, which ultimately may favor viral persistence.
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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.