Hypersusceptibility to vesicular stomatitis virus infection in Dicer1-deficient mice is due to impaired miR24 and miR93 expression

被引：321

作者：

Otsuka, Motoyuki

Jing, Qing

Georgel, Philippe

New, Liguo

Chen, Jianming

Mols, Johann

Kang, Young Jun

Jiang, Zhengfan

Du, Xin

Cook, Ryan

Das, Subash C.

Pattnaik, Asit K.

Beutler, Bruce

Han, Jiahuai ^{[1
]}

机构：

[1] Scripps Res Inst, Dept Immunol, La Jolla, CA 92037 USA

[2] Xiamen Univ, Sch Life Sci, Key Lab Minist Educ Cell Biol & Tumor Cell Engn, Xiamen 361005, Fujian, Peoples R China

[3] Chinese Acad Prevent Med, Shanghai Inst Biol Sci, Inst Hlth Sci, Shanghai 200025, Peoples R China

[4] Univ Nebraska, Dept Vet & Biomed Sci, Lincoln, NE 68588 USA

[5] Univ Nebraska, Nebraska Ctr Virol, Lincoln, NE 68588 USA

来源：

IMMUNITY | 2007年 / 27卷 / 01期

关键词：

D O I：

10.1016/j.immuni.2007.05.014

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

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.

引用

页码：123 / 134

页数：12

共 47 条

[1] The miRNA-processing enzyme dicer is essential for the morphogenesis and maintenance of hair follicles [J].