This Article Full Text Full Text (PDF) An author's correction has been published Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Fenner, B. J. Articles by Kwang, J. Search for Related Content PubMed PubMed Citation Articles by Fenner, B. J. Articles by Kwang, J.

 Previous Article  |  Next Article 

Journal of Virology, January 2006, p. 85-94, Vol. 80, No. 1
0022-538X/06/$08.00+0     doi:10.1128/JVI.80.1.85-94.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Betanodavirus B2 Is an RNA Interference Antagonist That Facilitates Intracellular Viral RNA Accumulation

Animal Health Biotechnology, Temasek Life Sciences Laboratory, National University of Singapore, Singapore 117604

Received 17 June 2005/ Accepted 23 September 2005

Betanodaviruses are small positive-sense bipartite RNA viruses that infect a wide variety of fish species and are notorious for causing lethal outbreaks in juvenile fish hatcheries worldwide. The function of a small nonstructural protein, B2, encoded by the subgenomic RNA3 of betanodaviruses, has remained obscure. Greasy grouper nervous necrosis virus, a betanodavirus model, was used to develop a facile DNA-based reverse genetics system that recapitulated the virus infection cycle, and we used this system to show that B2 is a small nonstructural protein that is essential for high level accumulation of viral RNA1 after RNA transfection of fish, mammalian, and avian cells. The defect in RNA1 accumulation in a B2 mutant was partially complemented by supplying B2 RNA in trans. Confocal analysis of the cellular distribution of B2 indicated that B2 is able to enter the nucleus and accumulates there during the late stages of GGNNV infection. Using human HeLa cells as a cellular RNA interference model, we found that B2 could efficiently antagonize RNA interference, which is a property shared by the distantly related alphanodavirus B2 proteins. This function provides appears to provide an explanation, at least in part, for why B2 mutant RNA1 is severely impaired in its intracellular accumulation.

This article has been cited by other articles:

• Zhang, X., Segers, G. C., Sun, Q., Deng, F., Nuss, D. L. (2008). Characterization of Hypovirus-Derived Small RNAs Generated in the Chestnut Blight Fungus by an Inducible DCL-2-Dependent Pathway. J. Virol. 82: 2613-2619 [Abstract] [Full Text]  
• Fenner, B. J., Goh, W., Kwang, J. (2007). Dissection of Double-Stranded RNA Binding Protein B2 from Betanodavirus. J. Virol. 81: 5449-5459 [Abstract] [Full Text]  
• Fenner, B. J., Goh, W., Kwang, J. (2006). Sequestration and Protection of Double-Stranded RNA by the Betanodavirus B2 Protein. J. Virol. 80: 6822-6833 [Abstract] [Full Text]