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 journalArticle

259 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 (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.

Original languageEnglish (US)
Pages (from-to)123-134
Number of pages12
JournalImmunity
Volume27
Issue number1
DOIs
StatePublished - Jul 27 2007

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Keywords

  • MICROBIO
  • MOLIMMUNO

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Infectious Diseases

Cite this

Otsuka, M., Jing, Q., Georgel, P., New, L., Chen, J., Mols, J., Kang, YJ., Jiang, Z., Du, X., Cook, R., Das, S. C., Pattnaik, A. K., Beutler, B., & Han, J. (2007). Hypersusceptibility to Vesicular Stomatitis Virus Infection in Dicer1-Deficient Mice Is Due to Impaired miR24 and miR93 Expression. Immunity, 27(1), 123-134. https://doi.org/10.1016/j.immuni.2007.05.014