ArticleJournal of virology2013
Mutations in the cytoplasmic domain of the Newcastle disease virus fusion protein confer hyperfusogenic phenotypes modulating viral replication and pathogenicity.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 20 papers, 1 of them a synthesis that pooled it.
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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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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
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.
- Insights into the multifunctionality of viral glycoproteins F and HN in the lifecycle and pathogenesis of Newcastle disease virus: a systematic review.Veterinary research · 2025Pooled it
- Molecular Characterization of Publicly Available NDV F Gene Sequences From Bangladesh (2010-2024).Veterinary medicine international · 2026Article
- Nucleotide sequence characterization, amino acid variations and 3D structural analysis of HN protein of the NDV VIId genotype.Veterinary medicine and science · 2024Article
- Mutagenesis of the di-leucine motif in the cytoplasmic tail of newcastle disease virus fusion protein modulates the viral fusion ability and pathogenesis.Virology journal · 2023Article
- Phylogeny and Pathogenicity of Subtype XIIb NDVs from Francolins in Southwestern China and Effective Protection by an Inactivated Vaccine.Transboundary and emerging diseases · 2023Article
- Adaptor complex-mediated trafficking of Newcastle disease virus fusion protein is regulated by the YLMY motif of its cytoplasmic tail.Virulence · 2022Article
- Contribution of mutation I142M in fusion protein and Q44R in matrix protein of Newcastle disease virus to virulence in ducks.The Journal of veterinary medical science · 2022Article
- Article
- Activation of the extracellular signal-regulated kinase pathway is required for replication of Newcastle disease virus.Archives of virology · 2021Article
- AvianFrontiers in veterinary science · 2021Review
- Residues 315 and 369 in HN Protein Contribute to the Thermostability of Newcastle Disease Virus.Frontiers in microbiology · 2020Article
- Article
- A Review of Functional Motifs Utilized by Viruses.Proteomes · 2016Review
- Host Innate Immune Responses of Ducks Infected with Newcastle Disease Viruses of Different Pathogenicities.Frontiers in microbiology · 2015Article
- Molecular pathotyping and phylogenesis of the first Newcastle disease virus strain isolated from backyard chickens in Qatar.Tropical animal health and production · 2015Article
- The Epstein-Barr virus (EBV) glycoprotein B cytoplasmic C-terminal tail domain regulates the energy requirement for EBV-induced membrane fusion.Journal of virology · 2014Article
- Paramyxovirus glycoprotein incorporation, assembly and budding: a three way dance for infectious particle production.Viruses · 2014Review
- Newcastle disease virus: current status and our understanding.Virus research · 2014Review
- Species based synonymous codon usage in fusion protein gene of Newcastle disease virus.PloS one · 2014Article
- Different regions of the newcastle disease virus fusion protein modulate pathogenicity.PloS one · 2014Article
Corrections and comments
- Correction · 2020-02-28Error in Image · Investigation by Company/Institution ·
- Erratum issued
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
The Newcastle disease virus (NDV) fusion protein (F) mediates fusion of viral and host cell membranes and is a major determinant of NDV pathogenicity. In the present study, we demonstrate the effects of functional properties of F cytoplasmic tail (CT) amino acids on virus replication and pathogenesis. Out of a series of C-terminal deletions in the CT, we were able to rescue mutant viruses lacking two or four residues (rΔ2 and rΔ4). We further rescued viral mutants with individual amino acid substitutions at each of these four terminal residues (rM553A, rK552A, rT551A, and rT550A). In addition, the NDV F CT has two conserved tyrosine residues (Y524 and Y527) and a dileucine motif (LL536-537). In other paramyxoviruses, these residues were shown to affect fusion activity and are central elements in basolateral targeting. The deletion of 2 and 4 CT amino acids and single tyrosine substitution resulted in hyperfusogenic phenotypes and increased viral replication and pathogenesis. We further found that in rY524A and rY527A viruses, disruption of the targeting signals did not reduce the expression on the apical or basolateral surface in polarized Madin-Darby canine kidney cells, whereas in double tyrosine mutant, it was reduced on both the apical and basolateral surfaces. Interestingly, in rL536A and rL537A mutants, the F protein expression was more on the apical than on the basolateral surface, and this effect was more pronounced in the rL537A mutant. We conclude that these wild-type residues in the NDV F CT have an effect on regulating F protein biological functions and thus modulating viral replication and pathogenesis.
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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.