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Journal of Virology, December 2007, p. 13816-13824, Vol. 81, No. 24
0022-538X/07/$08.00+0     doi:10.1128/JVI.02822-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Identification and Functional Analysis of Salmon Annexin 1 Induced by a Virus Infection in a Fish Cell Line

Hyun Jin Hwang,^1,3, Chang Hoon Moon,^2, Han Geun Kim,¹ Joo Yun Kim,¹ Jung Min Lee,¹ Jeong Woo Park,^2* and Dae Kyun Chung^1,3*

Graduate School of Biotechnology and Institute of Life Science and Resources, Kyung Hee University, Yongin 449-701, Korea,¹ Department of Biological Sciences, University of Ulsan, Ulsan 680-749, Korea,² RNA Inc., #308 College of Industry, Kyung Hee University, Yongin 449-701, Korea³

Received 20 December 2006/ Accepted 12 September 2007

In this study, we investigated changes in protein expression of fish cells induced by infection of infectious pancreatic necrosis virus (IPNV) using two-dimensional electrophoresis and matrix-assisted laser desorption-time of flight proton motive force analysis and identified a novel type of salmon annexin 1 that is induced in fish cells by infection with IPNV. Northern blotting showed that this annexin is overexpressed in IPNV-infected cells compared to control cells, and further analysis revealed that it has a 1,509-bp full-length cDNA sequence with an open reading frame encoding 339 amino acids (GenBank accession no. AY944135). Amino acid sequence analysis revealed that this protein belongs to the annexin 1 subfamily. By applying RNA interference, the mRNA levels of salmon annexin 1 were suppressed and, under these conditions, apoptosis of IPNV-infected cells was significantly increased. While small interfering RNA (siRNA) treatment did not affect the levels of the viral proteins significantly until 10 h postinfection, it reduced the titer of extracellular virus to 25% of that of a scrambled siRNA-treated control. These data provide evidence of an antiapoptotic function for salmon annexin 1 that is important for IPNV growth in cultured cells.

Published ahead of print on 19 September 2007.

H.J.H. and C.H.M. contributed equally to this work.