This Article Full Text Full Text (PDF) Other Versions of this Article: JVI.02635-07v1 82/13/6130    most recent 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 Google Scholar Articles by Nishio, M. Articles by Kolakofsky, D. PubMed PubMed Citation Articles by Nishio, M. Articles by Kolakofsky, D.

 Previous Article  |  Next Article 

Journal of Virology, July 2008, p. 6130-6138, Vol. 82, No. 13
0022-538X/08/$08.00+0     doi:10.1128/JVI.02635-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Human Parainfluenza Virus Type 2 V Protein Inhibits Genome Replication by Binding to the L Protein: Possible Role in Promoting Viral Fitness

Department of Microbiology, Mie University Graduate School of Medicine, 2-174, Edobashi, Tsu, Mie 514-8507, Japan,¹ Department of Microbiology and Molecular Medicine, University of Geneva School of Medicine, 11 Ave. De Champel, CH1211, Geneva, Switzerland²

Received 11 December 2007/ Accepted 6 April 2008

The human parainfluenza virus type 2 (hPIV2) V protein plays important roles in inhibiting the host interferon response and promoting virus growth, but its role in hPIV2 replication and transcription is not clear. A green fluorescent protein (GFP)-expressing a negative-sense minigenomic construct of hPIV2 has been established by standard technology, with helper plasmids expressing the nucleocapsid protein (NP), phosphoprotein (P), and large RNA polymerase (L) protein, to examine the role of V protein. We found that the simultaneous expression of wild-type V protein in the minigenome system inhibited GFP expression, at least in part, by inhibiting minigenome replication. In contrast, expression of C terminally truncated or mutant hPIV2 V proteins had no effect. Moreover, the V protein of simian virus 41, the rubulavirus most closely related virus to hPIV2, also inhibited GFP expression, whereas that of PIV5, a more distantly related rubulavirus, did not. Using these other rubulavirus V proteins, as well as various mutant hPIV2 V proteins, we found that the ability of V protein to inhibit GFP expression correlated with its ability to bind to L protein via its C-terminal V protein-specific region, but there was no correlation with NP binding. A possible role for this inhibition of genome replication in promoting viral fitness is discussed.

Published ahead of print on 16 April 2008.