This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Chan, Y.-L.
Right arrow Articles by Lin, Y.-L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Chan, Y.-L.
Right arrow Articles by Lin, Y.-L.

 Previous Article  |  Next Article 

Journal of Virology, November 2008, p. 10455-10464, Vol. 82, No. 21
0022-538X/08/$08.00+0     doi:10.1128/JVI.00438-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

The Cellular Antiviral Protein Viperin Is Attenuated by Proteasome-Mediated Protein Degradation in Japanese Encephalitis Virus-Infected Cells{triangledown}

Yi-Lin Chan,1,2 Tsung-Hsien Chang,2,{ddagger} Ching-Len Liao,1,3 and Yi-Ling Lin1,2,4*

Graduate Institute of Life Sciences,1 Department of Microbiology and Immunology, National Defense Medical Center,3 Institute of Biomedical Sciences,2 Genomics Research Center, Academia Sinica, Taipei, Taiwan, Republic of China4

Received 28 February 2008/ Accepted 21 August 2008

Viperin is identified as an antiviral protein induced by interferon (IFN), viral infections, and pathogen-associated molecules. In this study, we found that viperin is highly induced at the RNA level by Japanese encephalitis virus (JEV) and Sindbis virus (SIN) and that viperin protein is degraded in JEV-infected cells through a proteasome-dependent mechanism. Promoter analysis revealed that SIN induces viperin expression in an IFN-dependent manner but that JEV by itself activates the viperin promoter through IFN regulatory factor-3 and AP-1. The overexpression of viperin significantly decreased the production of SIN, but not of JEV, whereas the proteasome inhibitor MG132 sustained the protein level and antiviral effect of viperin in JEV-infected cells. Knockdown of viperin expression by RNA interference also enhanced the replication of SIN, but not that of JEV. Our results suggest that even though viperin gene expression is highly induced by JEV, it is negatively regulated at the protein level to counteract its antiviral effect. In contrast, SIN induces viperin through the action of IFN, and viperin exhibits potent antiviral activity against SIN.

* Corresponding author. Mailing address: Institute of Biomedical Sciences, Academia Sinica, No. 128, Sec. 2, Academy Road, Taipei 115, Taiwan, Republic of China. Phone: (886)-2-2652-3902. Fax: (886)-2-2785-8847. E-mail: yll{at}ibms.sinica.edu.tw

{triangledown} Published ahead of print on 3 September 2008.

{ddagger} Present address: 9000 Rockville Pike, NICHD, Building 6, Room 2A05, Bethesda, MD 20892.

Journal of Virology, November 2008, p. 10455-10464, Vol. 82, No. 21
0022-538X/08/$08.00+0     doi:10.1128/JVI.00438-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»