Hypersusceptibility to Vesicular Stomatitis Virus Infection in Dicer1-Deficient Mice Is Due to Impaired miR24 and miR93 Expression

Motoyuki Otsuka; Qing Jing; Philippe Georgel; Liguo New; Jianming Chen; Johann Mols; Young Jun Kang; Zhengfan Jiang; Xin Du; Ryan Cook; Subash C. Das; Asit K. Pattnaik; Bruce Beutler; Jiahuai Han

doi:10.1016/j.immuni.2007.05.014

Hypersusceptibility to Vesicular Stomatitis Virus Infection in Dicer1-Deficient Mice Is Due to Impaired miR24 and miR93 Expression

Motoyuki Otsuka, Qing Jing, Philippe Georgel, Liguo New, Jianming Chen, Johann Mols, Young Jun Kang, Zhengfan Jiang, Xin Du, Ryan Cook, Subash C. Das, Asit K. Pattnaik, Bruce Beutler, Jiahuai Han

Research output: Contribution to journal › Article › peer-review

306 Scopus citations

Abstract

Dicer is essential for plant, Caenorhabditis elegans, and Drosophila antiviral responses because of its role in generating small interfering RNA (siRNA) from viral genomes. We show that because of impaired miRNA production, mice with a variant Dicer1 allele (Dicer1^d/d) were more susceptible to vesicular stomatitis virus (VSV) infection. We did not detect VSV genome-derived siRNA in wild-type cells or any alteration of interferon-mediated antiviral responses by Dicer1 deficiency. Rather, we found that host miR24 and miR93 could target viral large protein (L protein) and phosphoprotein (P protein) genes, and a lack of miR24 and miR93 was responsible for increased VSV replication in Dicer1^d/d cells. Our data suggest that host miRNA can play a role in host interactions with viruses.

Original language	English (US)
Pages (from-to)	123-134
Number of pages	12
Journal	Immunity
Volume	27
Issue number	1
DOIs	https://doi.org/10.1016/j.immuni.2007.05.014
State	Published - Jul 27 2007

Keywords

MICROBIO
MOLIMMUNO

ASJC Scopus subject areas

Immunology and Allergy
Immunology
Infectious Diseases

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10.1016/j.immuni.2007.05.014

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title = "Hypersusceptibility to Vesicular Stomatitis Virus Infection in Dicer1-Deficient Mice Is Due to Impaired miR24 and miR93 Expression",

abstract = "Dicer is essential for plant, Caenorhabditis elegans, and Drosophila antiviral responses because of its role in generating small interfering RNA (siRNA) from viral genomes. We show that because of impaired miRNA production, mice with a variant Dicer1 allele (Dicer1d/d) were more susceptible to vesicular stomatitis virus (VSV) infection. We did not detect VSV genome-derived siRNA in wild-type cells or any alteration of interferon-mediated antiviral responses by Dicer1 deficiency. Rather, we found that host miR24 and miR93 could target viral large protein (L protein) and phosphoprotein (P protein) genes, and a lack of miR24 and miR93 was responsible for increased VSV replication in Dicer1d/d cells. Our data suggest that host miRNA can play a role in host interactions with viruses.",

keywords = "MICROBIO, MOLIMMUNO",

author = "Motoyuki Otsuka and Qing Jing and Philippe Georgel and Liguo New and Jianming Chen and Johann Mols and Young Jun Kang and Zhengfan Jiang and Xin Du and Ryan Cook and Das, {Subash C.} and Pattnaik, {Asit K.} and Bruce Beutler and Jiahuai Han",

note = "Funding Information: We thank Dr. Kaoru Saigo for Dicer antibodies, Dr. Carol Shoshkes Reiss for VSV antibodies, and Dr. Michael A. Whitt for the VSV antigenomic DNA. M.O. was supported by fellowships from the Sankyo Foundation of Life Science and the Uehara Memorial Foundation. This work was supported by National Institutes of Health grants GM67101, AI41637, and AI54696 and by 863 program grant AA02Z164. ",

year = "2007",

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day = "27",

doi = "10.1016/j.immuni.2007.05.014",

language = "English (US)",

volume = "27",

pages = "123--134",

journal = "Immunity",

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T1 - Hypersusceptibility to Vesicular Stomatitis Virus Infection in Dicer1-Deficient Mice Is Due to Impaired miR24 and miR93 Expression

AU - Otsuka, Motoyuki

AU - Jing, Qing

AU - Georgel, Philippe

AU - New, Liguo

AU - Chen, Jianming

AU - Mols, Johann

AU - Kang, Young Jun

AU - Jiang, Zhengfan

AU - Du, Xin

AU - Cook, Ryan

AU - Das, Subash C.

AU - Pattnaik, Asit K.

AU - Beutler, Bruce

AU - Han, Jiahuai

N1 - Funding Information: We thank Dr. Kaoru Saigo for Dicer antibodies, Dr. Carol Shoshkes Reiss for VSV antibodies, and Dr. Michael A. Whitt for the VSV antigenomic DNA. M.O. was supported by fellowships from the Sankyo Foundation of Life Science and the Uehara Memorial Foundation. This work was supported by National Institutes of Health grants GM67101, AI41637, and AI54696 and by 863 program grant AA02Z164.

PY - 2007/7/27

Y1 - 2007/7/27

N2 - Dicer is essential for plant, Caenorhabditis elegans, and Drosophila antiviral responses because of its role in generating small interfering RNA (siRNA) from viral genomes. We show that because of impaired miRNA production, mice with a variant Dicer1 allele (Dicer1d/d) were more susceptible to vesicular stomatitis virus (VSV) infection. We did not detect VSV genome-derived siRNA in wild-type cells or any alteration of interferon-mediated antiviral responses by Dicer1 deficiency. Rather, we found that host miR24 and miR93 could target viral large protein (L protein) and phosphoprotein (P protein) genes, and a lack of miR24 and miR93 was responsible for increased VSV replication in Dicer1d/d cells. Our data suggest that host miRNA can play a role in host interactions with viruses.

AB - Dicer is essential for plant, Caenorhabditis elegans, and Drosophila antiviral responses because of its role in generating small interfering RNA (siRNA) from viral genomes. We show that because of impaired miRNA production, mice with a variant Dicer1 allele (Dicer1d/d) were more susceptible to vesicular stomatitis virus (VSV) infection. We did not detect VSV genome-derived siRNA in wild-type cells or any alteration of interferon-mediated antiviral responses by Dicer1 deficiency. Rather, we found that host miR24 and miR93 could target viral large protein (L protein) and phosphoprotein (P protein) genes, and a lack of miR24 and miR93 was responsible for increased VSV replication in Dicer1d/d cells. Our data suggest that host miRNA can play a role in host interactions with viruses.

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Hypersusceptibility to Vesicular Stomatitis Virus Infection in Dicer1-Deficient Mice Is Due to Impaired miR24 and miR93 Expression

Abstract

Keywords

ASJC Scopus subject areas

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