Modulation of hepatitis C virus RNA abundance by a liver-specific MicroRNA Public Deposited

Downloadable Content

Download PDF
Creator
  • Lemon, Stanley M.
    • Other Affiliation: Center for Hepatitis Research, Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555-1019, USA
  • Yi, MinKyung
    • Other Affiliation: Center for Hepatitis Research, Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555-1019, USA
  • Jopling, Catherine L.
    • Other Affiliation: Department of Microbiology and Immunology, Stanford University, Stanford, CA 94305, USA
  • Lancaster, Alissa M.
    • Other Affiliation: Department of Microbiology and Immunology, Stanford University, Stanford, CA 94305, USA
  • Sarnow, Peter
    • Other Affiliation: Department of Microbiology and Immunology, Stanford University, Stanford, CA 94305, USA
Abstract
  • MicroRNAs are small RNA molecules that regulate messenger RNA (mRNA) expression. MicroRNA 122 (miR-122) is specifically expressed and highly abundant in the human liver. We show that the sequestration of miR-122 in liver cells results in marked loss of autonomously replicating hepatitis C viral RNAs. A genetic interaction between miR-122 and the 5′ noncoding region of the viral genome was revealed by mutational analyses of the predicted microRNA binding site and ectopic expression of miR-122 molecules containing compensatory mutations. Studies with replication-defective RNAs suggested that miR-122 did not detectably affect mRNA translation or RNA stability. Therefore, miR-122 is likely to facilitate replication of the viral RNA, suggesting that miR-122 may present a target for antiviral intervention.
Date of publication
Identifier
  • 2-s2.0-24644483623
  • doi:10.1126/science.1113329
Related resource URL
Resource type
  • Article
Rights statement
  • In Copyright
Journal title
  • Science
Journal volume
  • 309
Journal issue
  • 5740
Page start
  • 1577
Page end
  • 1581
Language
  • English
Version
  • Postprint
ISSN
  • 0036-8075
Parents:

This work has no parents.

Items