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Published online ahead of print on 4 March 2009 as doi:10.1099/vir.0.009415-0
Journal of General Virology 2009;90:1670.

A more recent version of this article appeared on July 1, 2009 J Gen Virol (2009), DOI 10.1099/vir.0.009415-0
© 2009 Society for General Microbiology

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Genomic expression profiling of peripheral blood leukocytes of pigs infected with highly virulent classical swine fever virus strain Shimen

Zixue Shi, Jinfu Sun, Huancheng Guo and Changchun Tu1

Institute of Veterinary Sciences, Academy of Military Medical Sciences

1 E-mail: changchun_tu{at}hotmail.com

Classical swine fever (CSF), caused by a virus of the same name (CSFV), is a highly contagious swine pyrexic disease featuring extensive hemorrhagic lesions and leukopenia, but little is known about the molecular mechanisms of its pathogenesis. To gain insight into the interaction between virus and host cells, microarray analyses were performed to detect alterations in genomic expression of pig peripheral blood leukocytes (PBL) following CSFV infection. Three healthy pigs were inoculated with a lethal dose of highly virulent CSFV strain Shimen. PBL were isolated at the onset of typical clinical signs and total RNA was subjected to microarray analyses with Affymetrix Porcine Genome Array GeneChips. Of all 20,201 pig genes arrayed in the chip, 1,745 showed altered expression (up- or down-regulation) after infection. These were classified into eight functional groups, relating to cell proliferation (3.6 %), immune response (2.1 %), apoptosis (1.4 %), kinase activity (1.4 %), signal transduction (1.4 %), transcription (0.7 %), receptor activity (0.7 %), and cytokines/chemokines (0.4 %). The remaining 88.3 % had unknown functions. Alterations in genomic expression were confirmed by real time RT-PCR of selected cellular genes and Western blot of annexin 2, a cellular protein relating to viral infection. The observed expression changes of numerous genes involved in immune and inflammatory responses and in the apoptosis process indicate that CSFV has developed sophisticated mechanisms to cause leukopenia in infected pigs. These data provide a basis for exploring the molecular pathogenesis of CSFV infection through an understanding of the interaction between viral and cellular components.

Received 4 December 2008; accepted 4 March 2009.





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