ArticleFrontiers in cellular and infection microbiology2018
Newcastle Disease Virus V Protein Inhibits Cell Apoptosis and Promotes Viral Replication by Targeting CacyBP/SIP.
Article in Frontiers in cellular and infection microbiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.
- The multifaceted interactions between Newcastle disease virus proteins and host proteins: a systematic review.Virulence · 2024Pooled it
- Decoding the diversity: a comprehensive sequence analysis of accessory viral protein W of Newcastle disease virus.Journal of biosciences · 2026Article
- Identification of β4GALNT2 as an anti-hPIV3 factor through genome-wide CRISPR/Cas9 library screening.Emerging microbes & infections · 2025Article
- Time-Resolved Analysis of Protein-Protein Ensembles Using a Destabilizing Domain to Map Dynamic Interactions of SARS-CoV-2 nsp15.ACS chemical biology · 2025Article
- Genome-Wide Screening Reveals the Oncolytic Mechanism of Newcastle Disease Virus in a Human Colonic Carcinoma Cell Line.Viruses · 2025Article
- Accessory viral protein, V, of Newcastle Disease Virus binds dsRNA to facilitate immune evasion.Virusdisease · 2025Article
- Non-Structural Protein V of Canine Distemper Virus Induces Autophagy via PI3K/AKT/mTOR Pathway to Facilitate Viral Replication.International journal of molecular sciences · 2024Article
- PBLD promotes IRF3 mediated the type I interferon (IFN-I) response and apoptosis to inhibit viral replication.Cell death & disease · 2024Article
- Mammalian orthoreovirus capsid protein σ3 antagonizes RLR-mediated antiviral responses by degrading MAVS.mSphere · 2024Article
- Review
- Article
- Molecular characterization suggests kinetic modulation of expression of accessory viral protein, W, in Newcastle disease virus infected DF1 cells.Virusdisease · 2023Article
- The V protein in oncolytic Newcastle disease virus promotes HepG2 hepatoma cell proliferation at the single-cell level.BMC cancer · 2023Article
- Pathologic Mechanisms of the Newcastle Disease Virus.Viruses · 2023Review
- The production of Newcastle disease virus-like particles inFrontiers in plant science · 2023Article
- Detection of Velogenic Avian Paramyxoviruses in Rock Doves in New York City, New York.Microbiology spectrum · 2022Article
- Activation of the extracellular signal-regulated kinase pathway is required for replication of Newcastle disease virus.Archives of virology · 2021Article
- Evasion of Host Antiviral Innate Immunity by Paramyxovirus Accessory Proteins.Frontiers in microbiology · 2021Review
- Genomic Diversity and Evolution of Quasispecies in Newcastle Disease Virus Infections.Viruses · 2020Article
- Screening and mechanistic study of key sites of the hemagglutinin-neuraminidase protein related to the virulence of Newcastle disease virus.Poultry science · 2020Article
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Newcastle disease virus (NDV) has been classified by the World Organization for Animal Health (OIE) as a notable disease-causing virus, and this virus has the ability to infect a wide range of birds. V protein is a non-structural protein of NDV. V protein has been reported to inhibit cell apoptosis (Park et al., 2003a) and promote viral replication (Huang et al., 2003), however, the mechanisms of action of V protein have not been elucidated. In the present study, a yeast two-hybrid screen was performed, and V protein was found to interact with the CacyBP/SIP protein. The results of co-immunoprecipitation and immuno-colocalization assays confirmed the interaction between V protein and CacyBP/SIP. The results of quantitative-PCR and viral plaque assays showed that overexpression of CacyBP/SIP inhibited viral replication in DF-1 cells. Overexpression of CacyBP/SIP in DF-1 cells induced caspase3-dependent apoptosis. The effect of knocking down CacyBP/SIP by siRNA was the opposite of that observed upon overexpression. Moreover, it is known that NDV induces cell apoptosis via multiple caspase-dependent pathways. Furthermore, V protein inhibited cell apoptosis and downregulated CacyBP/SIP expression in DF-1 cells. Taken together, the findings of the current study indicate that V protein interacts with CacyBP/SIP, thereby regulating cell apoptosis and viral replication.
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