DDX3 DEAD-Box RNA Helicase Is Required for Hepatitis C Virus RNA Replication
Open Access
- 15 December 2007
- journal article
- research article
- Published by American Society for Microbiology in Journal of Virology
- Vol. 81 (24), 13922-13926
- https://doi.org/10.1128/jvi.01517-07
Abstract
DDX3, a DEAD-box RNA helicase, binds to the hepatitis C virus (HCV) core protein. However, the role(s) of DDX3 in HCV replication is still not understood. Here we demonstrate that the accumulation of both genome-length HCV RNA (HCV-O, genotype 1b) and its replicon RNA were significantly suppressed in HuH-7-derived cells expressing short hairpin RNA targeted to DDX3 by lentivirus vector transduction. As well, RNA replication of JFH1 (genotype 2a) and release of the core into the culture supernatants were suppressed in DDX3 knockdown cells after inoculation of the cell culture-generated HCVcc. Thus, DDX3 is required for HCV RNA replication.Keywords
This publication has 28 references indexed in Scilit:
- Subproteomic analysis of the cellular proteins associated with the 3′ untranslated region of the hepatitis C virus genome in human liver cellsBiochemical and Biophysical Research Communications, 2006
- Identification of Two Gene Variants Associated With Risk of Advanced Fibrosis in Patients With Chronic Hepatitis CGastroenterology, 2006
- The DEAD-box protein family of RNA helicasesGene, 2005
- DDX3, a DEAD box RNA helicase, is deregulated in hepatitis virus-associated hepatocellular carcinoma and is involved in cell growth controlOncogene, 2005
- Viral and cellular RNA helicases as antiviral targetsNature Reviews Drug Discovery, 2005
- Production of infectious hepatitis C virus in tissue culture from a cloned viral genomeNature Medicine, 2005
- Efficient replication of a full-length hepatitis C virus genome, strain O, in cell culture, and development of a luciferase reporter systemBiochemical and Biophysical Research Communications, 2005
- Requirement of DDX3 DEAD Box RNA Helicase for HIV-1 Rev-RRE Export FunctionCell, 2004
- Induction of an interferon response by RNAi vectors in mammalian cellsNature Genetics, 2003
- Functional Cross-Talk of HIV-1 Tat with p53 through Its C-Terminal DomainBiochemical and Biophysical Research Communications, 2001