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Zika Virus Non-Coding RNAs Antagonize Antiviral Responses by PKR-Mediated Translational Arrest (Ribo-Seq)

ABSTRACT: Zika Virus Non-Coding RNAs Antagonize Antiviral Responses by PKR-Mediated Translational Arrest (Ribo-Seq)

PROVIDER: PRJNA1069085 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27731317.fastq.gz	Fastqsanger.gz
	SRR27731318.fastq.gz	Fastqsanger.gz
	SRR27731319.fastq.gz	Fastqsanger.gz
	SRR27731320.fastq.gz	Fastqsanger.gz
	SRR27731321.fastq.gz	Fastqsanger.gz

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Zika Virus Non-Coding RNAs Antagonize Antiviral Responses by PKR-Mediated Translational Arrest

Project description:Zika Virus Non-Coding RNAs Antagonize Antiviral Responses by PKR-Mediated Translational Arrest

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Zika Virus Non-Coding RNAs Antagonize Antiviral Responses by PKR-Mediated Translational Arrest (Ribo-Seq)

Project description:Zika virus (ZIKV) is an emerging mosquito-borne flavivirus that causes severe outbreaks in human populations. ZIKV infection leads to the accumulation of small non-coding viral RNAs (known as sfRNAs) that are crucial for evasion of antiviral responses and for viral pathogenesis. However, the mechanistic understanding of how sfRNAs function remains incomplete. Here, we use recombinant ZIKVs and ribosome profiling of infected human cells to show that sfRNAs block translation of antiviral genes. Mechanistically, we demonstrate that specific RNA structures present in sfRNAs trigger PKR activation, which instead of limiting viral replication, enhances viral particle production. Although ZIKV infection induces mRNA expression of antiviral genes, translation efficiency of type I interferon and interferon stimulated genes were significantly downregulated by PKR activation. Our results reveal a novel viral adaptation mechanism mediated by sfRNAs, where ZIKV increases its fitness by repurposing the antiviral role of PKR into a proviral factor.

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Zika Virus Non-Coding RNAs Antagonize Antiviral Responses by PKR-Mediated Translational Arrest (RNA-Seq)

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Zika Virus Non-Coding RNAs Antagonize Antiviral Responses by PKR-Mediated Translational Arrest

Project description:This SuperSeries is composed of the SubSeries listed below.

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Antagonism of mitophagy by Zika virus reveals Ajuba as a regulator of PINK1-Parkin signaling and PKR-dependent inflammation

Project description:Dysregulated inflammation is a key driver of disease following infection with the globally important human pathogens, Zika virus (ZIKV) and dengue virus. However, specific mechanisms of inflammation are not well defined. Here, we demonstrate that ZIKV antagonizes mitophagy, or the process of selective degradation of damaged mitochondria. The mechanism of antagonism was through interactions between NS5 and the host protein Ajuba to prevent Ajuba translocation to depolarized mitochondria. We further identify a role of Ajuba in mitophagy through augmenting PINK1 kinase activity. Mitophagy suppression in infected Ajuba-/- cells amplified the cellular integrated stress response (ISR) to promote ZIKV replication, and increased pro-inflammatory cytokine expression dependent on the ISR kinase, PKR. Thus, ZIKV suppresses mitophagy to favor replication and this failure of mitochondrial quality control is translated to inflammation by PKR, suggesting new therapeutic targets to treat flavivirus disease.

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PKR overexpression

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