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Newcastle disease virus triggers autophagy in U251 glioma cells to enhance virus replication.

Abstract
Newcastle disease virus (NDV) can replicate in tumor cells and induce apoptosis in late stages of infection. However, the interaction between NDV and cells in early stages of infection is not well understood. Here, we report that, shortly after infection, NDV triggers the formation of autophagosomes in U251 glioma cells, as demonstrated by an increased number of double-membrane vesicles, GFP-microtubule-associated protein 1 light chain 3 (GFP-LC3) a dot formations, and elevated production of LC3II. Moreover, modulation of NDV-induced autophagy by rapamycin, chloroquine or small interfering RNAs targeting the genes critical for autophagosome formation (Atg5 and Beclin-1) affects virus production, indicating that autophagy may be utilized by NDV to facilitate its own production. Furthermore, the class III phosphatidylinositol 3-kinase (PI3K)/Beclin-1 pathway plays a role in NDV-induced autophagy and virus production. Collectively, our data provide a unique example of a paramyxovirus that uses autophagy to enhance its production.
AuthorsChunchun Meng, Zhizhi Zhou, Ke Jiang, Shengqing Yu, Lijun Jia, Yantao Wu, Yanqing Liu, Songshu Meng, Chan Ding
JournalArchives of virology (Arch Virol) Vol. 157 Issue 6 Pg. 1011-8 (Jun 2012) ISSN: 1432-8798 [Electronic] Austria
PMID22398914 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • ATG5 protein, human
  • Apoptosis Regulatory Proteins
  • Autophagy-Related Protein 5
  • BECN1 protein, human
  • Beclin-1
  • Membrane Proteins
  • Microtubule-Associated Proteins
Topics
  • Animals
  • Apoptosis Regulatory Proteins (genetics, metabolism)
  • Autophagy
  • Autophagy-Related Protein 5
  • Beclin-1
  • Cell Line, Tumor
  • Glioma (genetics, physiopathology, therapy, virology)
  • Humans
  • Membrane Proteins (genetics, metabolism)
  • Microtubule-Associated Proteins (genetics, metabolism)
  • Newcastle disease virus (genetics, physiology)
  • Oncolytic Virotherapy
  • Virus Replication

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