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Nucleic Acids Symposium Series 2004 48(1):307-308; doi:10.1093/nass/48.1.307
© 2004 by Oxford University Press
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RNAi expression mediated inhibition of HCV replication

Hiroyuki Hamazaki1, Saneyuki Ujino1, Emi Abe1, Naoko Miyano-Kurosaki1,2, Kunitada Shimotohno3 and Hiroshi Takaku1,2

1 Department of Life and Environmental Sciences, Chiba Institute of Technology, 2-17-1 Tsudanuma, Narashino, Chiba 275-0016, Japan, 2 High Technology Research Center, Chiba Institute of Technology, 2-17-1 Tsudanuma, Narashino, Chiba 275-0016, Japan, 3 Department of Viral Oncology, Institute for Virus Research, Kyoto University, 53 Kawara-cho, Shogo-in, Sakyo-ku, Kyoto 606-8507, Japan

The RNA interference (RNAi) mechanism is a recently observed process in which the introduction of a double-stranded RNA (dsRNA) into a cell causes the specific degradation of an mRNA containing the same sequence. The 21–23nt guide RNAs, generated by RNase III cleavage from longer dsRNAs, are associated with sequence-specific mRNA degradation. Here, we show that vector derived dsRNA specifically inhibit the replication of HCV RNA in HCV replicon cells. We designed a long dsRNA targeted to the full length HCV IRES region (1–377nt). Real Time RT-PCR was performed with a TaqMan RT-PCR, to solely amplify and enable quantification of HCV RNA. Our results indicated HCV replication reduction to near background levels in a sequence-specific manner by the long-dsRNAs in the HCV replicon cells.

Our results support the potential of using siRNA gene therapy to inhibit HCV replication, which may prove to be valuable in the treatment of hepatitis C.


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