Deletion of Cytoplasmic Double-Stranded RNA Sensors Does Not Uncover Viral Small Interfering RNA Production in Human Cells

ABSTRACT Antiviral immunity in insects and plants is mediated by the RNA interference (RNAi) pathway in which viral long double-stranded RNA (dsRNA) is processed into small interfering RNAs (siRNAs) by Dicer enzymes. Although this pathway is evolutionarily conserved, its involvement in antiviral def...

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Autores principales:	Susan Schuster, Lotte E. Tholen, Gijs J. Overheul, Frank J. M. van Kuppeveld, Ronald P. van Rij
Formato:	article
Lenguaje:	EN
Publicado:	American Society for Microbiology 2017
Materias:	RNA interference RNA virus innate immunity Microbiology QR1-502
Acceso en línea:	https://doaj.org/article/03a486fa50d143b2871fcedda04b4d12
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spelling	oai:doaj.org-article:03a486fa50d143b2871fcedda04b4d122021-11-15T15:22:05ZDeletion of Cytoplasmic Double-Stranded RNA Sensors Does Not Uncover Viral Small Interfering RNA Production in Human Cells10.1128/mSphere.00333-172379-5042https://doaj.org/article/03a486fa50d143b2871fcedda04b4d122017-08-01T00:00:00Zhttps://journals.asm.org/doi/10.1128/mSphere.00333-17https://doaj.org/toc/2379-5042ABSTRACT Antiviral immunity in insects and plants is mediated by the RNA interference (RNAi) pathway in which viral long double-stranded RNA (dsRNA) is processed into small interfering RNAs (siRNAs) by Dicer enzymes. Although this pathway is evolutionarily conserved, its involvement in antiviral defense in mammals is the subject of debate. In vertebrates, recognition of viral RNA induces a sophisticated type I interferon (IFN)-based immune response, and it has been proposed that this response masks or inhibits antiviral RNAi. To test this hypothesis, we analyzed viral small RNA production in differentiated cells deficient in the cytoplasmic RNA sensors RIG-I and MDA5. We did not detect 22-nucleotide (nt) viral siRNAs upon infection with three different positive-sense RNA viruses. Our data suggest that the depletion of cytoplasmic RIG-I-like sensors is not sufficient to uncover viral siRNAs in differentiated cells. IMPORTANCE The contribution of the RNA interference (RNAi) pathway in antiviral immunity in vertebrates has been widely debated. It has been proposed that RNAi possesses antiviral activity in mammalian systems but that its antiviral effect is masked by the potent antiviral interferon response in differentiated mammalian cells. In this study, we show that inactivation of the interferon response is not sufficient to uncover antiviral activity of RNAi in human epithelial cells infected with three wild-type positive-sense RNA viruses.Susan SchusterLotte E. TholenGijs J. OverheulFrank J. M. van KuppeveldRonald P. van RijAmerican Society for MicrobiologyarticleRNA interferenceRNA virusinnate immunityMicrobiologyQR1-502ENmSphere, Vol 2, Iss 4 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	RNA interference RNA virus innate immunity Microbiology QR1-502
spellingShingle	RNA interference RNA virus innate immunity Microbiology QR1-502 Susan Schuster Lotte E. Tholen Gijs J. Overheul Frank J. M. van Kuppeveld Ronald P. van Rij Deletion of Cytoplasmic Double-Stranded RNA Sensors Does Not Uncover Viral Small Interfering RNA Production in Human Cells
description	ABSTRACT Antiviral immunity in insects and plants is mediated by the RNA interference (RNAi) pathway in which viral long double-stranded RNA (dsRNA) is processed into small interfering RNAs (siRNAs) by Dicer enzymes. Although this pathway is evolutionarily conserved, its involvement in antiviral defense in mammals is the subject of debate. In vertebrates, recognition of viral RNA induces a sophisticated type I interferon (IFN)-based immune response, and it has been proposed that this response masks or inhibits antiviral RNAi. To test this hypothesis, we analyzed viral small RNA production in differentiated cells deficient in the cytoplasmic RNA sensors RIG-I and MDA5. We did not detect 22-nucleotide (nt) viral siRNAs upon infection with three different positive-sense RNA viruses. Our data suggest that the depletion of cytoplasmic RIG-I-like sensors is not sufficient to uncover viral siRNAs in differentiated cells. IMPORTANCE The contribution of the RNA interference (RNAi) pathway in antiviral immunity in vertebrates has been widely debated. It has been proposed that RNAi possesses antiviral activity in mammalian systems but that its antiviral effect is masked by the potent antiviral interferon response in differentiated mammalian cells. In this study, we show that inactivation of the interferon response is not sufficient to uncover antiviral activity of RNAi in human epithelial cells infected with three wild-type positive-sense RNA viruses.
format	article
author	Susan Schuster Lotte E. Tholen Gijs J. Overheul Frank J. M. van Kuppeveld Ronald P. van Rij
author_facet	Susan Schuster Lotte E. Tholen Gijs J. Overheul Frank J. M. van Kuppeveld Ronald P. van Rij
author_sort	Susan Schuster
title	Deletion of Cytoplasmic Double-Stranded RNA Sensors Does Not Uncover Viral Small Interfering RNA Production in Human Cells
title_short	Deletion of Cytoplasmic Double-Stranded RNA Sensors Does Not Uncover Viral Small Interfering RNA Production in Human Cells
title_full	Deletion of Cytoplasmic Double-Stranded RNA Sensors Does Not Uncover Viral Small Interfering RNA Production in Human Cells
title_fullStr	Deletion of Cytoplasmic Double-Stranded RNA Sensors Does Not Uncover Viral Small Interfering RNA Production in Human Cells
title_full_unstemmed	Deletion of Cytoplasmic Double-Stranded RNA Sensors Does Not Uncover Viral Small Interfering RNA Production in Human Cells
title_sort	deletion of cytoplasmic double-stranded rna sensors does not uncover viral small interfering rna production in human cells
publisher	American Society for Microbiology
publishDate	2017
url	https://doaj.org/article/03a486fa50d143b2871fcedda04b4d12
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Deletion of Cytoplasmic Double-Stranded RNA Sensors Does Not Uncover Viral Small Interfering RNA Production in Human Cells

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