NDLI: NF90 exerts antiviral activity through regulation of PKR phosphorylation and stress granules in infected cells.

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NF90 exerts antiviral activity through regulation of PKR phosphorylation and stress granules in infected cells.

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NF90 exerts antiviral activity through regulation of PKR phosphorylation and stress granules in infected cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Song, Wenjun Lau, Siu-Ying Jin, Dong-Yan Mok, Bobo Wing-Yee Chen, Yixin Wang, Pui Huang, Xiaofeng Yuen, Kwok-Yung Wen, Xi Zheng, Min Chen, Honglin
Description	Author Affiliation: Wen X ( State Key Laboratory for Emerging Infectious Diseases, Department of Microbiology, The University of Hong Kong, Hong Kong Special Administrative Region, People's Republic of China)
Abstract	NF90 was shown to exhibit broad antiviral activity against several viruses, but detailed mechanisms remain unclear. In this study, we examined the molecular basis for the inhibitory effect of NF90 on virus replication mediated through protein kinase (PKR)-associated translational regulation. We first verified the interaction between NF90 and PKR in mammalian cells and showed that NF90 interacts with PKR through its C-terminal and that the interaction is independent of NF90 RNA-binding properties. We further showed that knockdown of NF90 resulted in significantly lower levels of PKR phosphorylation in response to dsRNA induction and influenza virus infection. We also showed that high concentrations of NF90 exhibit negative regulatory effects on PKR phosphorylation, presumably through competition for dsRNA via the C-terminal RNA-binding domain. PKR activation is essential for the formation of stress granules in response to dsRNA induction. Our results showed that NF90 is a component of stress granules. In NF90-knockdown cells, dsRNA treatment induced significantly lower levels of stress granules than in control cells. Further evidence for an NF90-PKR antiviral pathway was obtained using an NS1 mutated influenza A virus specifically attenuated in its ability to inhibit PKR activation. This mutant virus replicated indistinguishably from wild-type virus in NF90-knockdown cells, but not in scrambled control cells or Vero cells, indicating that NF90's antiviral function occurs through interaction with PKR. Taken together, these results reveal a yet-to-be defined host antiviral mechanism in which NF90 upregulation of PKR phosphorylation restricts virus infection.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	8
Volume Number	192
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2014-04-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Antiviral Agents Metabolism Cytoplasmic Granules Nuclear Factor 90 Proteins Stress, Physiological Eif-2 Kinase Animals Enzyme Activation Gene Expression Gene Knockdown Techniques Influenza A Virus Genetics Interferon-beta Models, Biological Mutation Phosphorylation Protein Binding Protein Transport Rna, Double-stranded Rna-binding Proteins Virus Replication Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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