Dengue virus infection induces formation of G3BP1 granules in human lung epithelial cells

Dengue virus infection induces formation of G3BP1 granules in human lung epithelial cells Cells reprogram ongoing translation in response to viral infection, resulting in formation of stress granules (SGs), while viruses have evolved a variety of strategies to antagonize the host SG response. Previous literature reported that in BHK-1 cells, infection with dengue virus (DENV) interfered with the SG formation. In the current study, we further investigated SG formation in human epithelial A549 cells by detecting subcellular localization of two SG hallmarks, TIA-1 and G3BP1. In response to DENV type 2 (DENV2) and type 3 (DENV3) infection, G3BP1, but not TIA-1, was recruited into cytoplasmic granules in some cells, and viral protein synthesis was significantly impaired in the G3BP1-granule-containing cells. Knockdown of G3BP1 significantly rescued the dsRNA-mediated suppression of DENV2 replication. Furthermore, our data showed that the phosphorylation of protein kinase regulated by dsRNA (PKR) and eIF2α, as well as accumulation of dsRNA, mainly occurred at the late stage of viral infection. This work revealed that in DENV-infected A549 cells, G3BP1 granules were assembled independently of TIA-1 and had a negative impact on viral replication. This extends our understanding of the antagonistic relationship between the SG response and dengue virus infection. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Archives of Virology Springer Journals

Dengue virus infection induces formation of G3BP1 granules in human lung epithelial cells

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Publisher
Springer Journals
Copyright
Copyright © 2015 by Springer-Verlag Wien
Subject
Biomedicine; Virology; Medical Microbiology; Infectious Diseases
ISSN
0304-8608
eISSN
1432-8798
D.O.I.
10.1007/s00705-015-2578-9
Publisher site
See Article on Publisher Site

Abstract

Cells reprogram ongoing translation in response to viral infection, resulting in formation of stress granules (SGs), while viruses have evolved a variety of strategies to antagonize the host SG response. Previous literature reported that in BHK-1 cells, infection with dengue virus (DENV) interfered with the SG formation. In the current study, we further investigated SG formation in human epithelial A549 cells by detecting subcellular localization of two SG hallmarks, TIA-1 and G3BP1. In response to DENV type 2 (DENV2) and type 3 (DENV3) infection, G3BP1, but not TIA-1, was recruited into cytoplasmic granules in some cells, and viral protein synthesis was significantly impaired in the G3BP1-granule-containing cells. Knockdown of G3BP1 significantly rescued the dsRNA-mediated suppression of DENV2 replication. Furthermore, our data showed that the phosphorylation of protein kinase regulated by dsRNA (PKR) and eIF2α, as well as accumulation of dsRNA, mainly occurred at the late stage of viral infection. This work revealed that in DENV-infected A549 cells, G3BP1 granules were assembled independently of TIA-1 and had a negative impact on viral replication. This extends our understanding of the antagonistic relationship between the SG response and dengue virus infection.

Journal

Archives of VirologySpringer Journals

Published: Dec 1, 2015

References

  • The role of posttranslational modifications in the assembly of stress granules
    Ohn, T; Anderson, P
  • Formation of stress granules inhibits apoptosis by suppressing stress-responsive MAPK pathways
    Arimoto, K; Fukuda, H; Imajoh-Ohmi, S; Saito, H; Takekawa, M
  • Regulation of stress granules and P-bodies during RNA virus infection
    Lloyd, RE
  • Innate immunity evasion by dengue virus
    Morrison, J; Aguirre, S; Fernandez-Sesma, A
  • Innate immunity to dengue virus infection and subversion of antiviral responses
    Green, AM; Beatty, PR; Hadjilaou, A; Harris, E
  • Mammalian stress granules represent sites of accumulation of stalled translation initiation complexes
    Kimball, SR; Horetsky, RL; Ron, D; Jefferson, LS; Harding, HP

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