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Journal of Virology, June 2007, p. 6122-6127, Vol. 81, No. 11
0022-538X/07/$08.00+0 doi:10.1128/JVI.02768-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Department of Neurology,1 Center for Biochemistry, University of Cologne, D-50931 Cologne, Germany,2 Laboratory of Virology, Department of Plant Sciences, Wageningen University, 6709 PD Wageningen, The Netherlands3
Received 15 December 2006/ Accepted 9 March 2007
Baculovirus DNA binding protein (DBP) binds preferentially single-stranded DNA in vitro and colocalizes with viral DNA replication sites. Here, its putative role as viral replication factor has been addressed by RNA interference. Silencing of DBP in Autographa californica multiple nucleopolyhedrovirus-infected cells increased expression of LEF-3, LEF-4, and P35. In contrast, expression of the structural genes coding for P39 and polyhedrin was suppressed while expression of genes coding for P10 and GP64 was unaffected. In the absence of DBP, viral DNA replication sites were formed, indicating replication of viral DNA. Electron microscopy studies, however, revealed a loss of formation of polyhedra and virus envelopment, suggesting that the primary role of DBP is viral formation rather than viral DNA replication.
Published ahead of print on 21 March 2007.
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