Hypersusceptibility to vesicular stomatitis virus infection in Dicer1-deficient mice is due to impaired miR24 and miR93 expression
Hypersusceptibility to vesicular stomatitis virus infection in Dicer1-deficient mice is due to impaired miR24 and miR93 expression
复制标题
DOI：
10.1016/j.immuni.2007.05.014
复制
发表时间：
2007-07-01
期刊：
影响因子：
32.4
通讯作者：
Han, Jiahuai
中科院分区：
文献类型：
--
作者：
Otsuka, Motoyuki;Jing, Qing;Han, Jiahuai
Dicer是植物、秀丽隐杆线虫和果蝇抗病毒反应所必需的，因为它在从病毒基因组产生小干扰RNA（siRNA）中起作用。我们发现，由于miRNA的产生受损，具有变异Dicer 1等位基因（Dicer 1（d/d））的小鼠更容易受到水泡性口炎病毒（VSV）感染。我们没有在野生型细胞中检测到VSV基因组来源的siRNA，也没有检测到Dicer 1缺陷导致干扰素介导的抗病毒反应的任何改变。相反，我们发现宿主miR 24和miR 93可以靶向病毒大蛋白（L蛋白）和磷蛋白（P蛋白）基因，并且miR 24和miR 93的缺乏是Dicer 1（d/d）细胞中VSV复制增加的原因。我们的数据表明，宿主miRNA可以在宿主与病毒的相互作用中发挥作用。
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.