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Drosophila melanogaster Mounts a Unique Immune Response to the Rhabdovirus Sigma virus

C. W. Tsai,^1, E. A. McGraw,² E.-D. Ammar,¹ R. G. Dietzgen,³ and S. A. Hogenhout^1,4*

Department of Entomology, The Ohio State University-OARDC, Wooster, Ohio 44691,¹ School of Integrative Biology, The University of Queensland, St. Lucia, Queensland 4072, Australia,² Department of Primary Industries and Fisheries, Emerging Technologies, Queensland Agricultural Biotechnology Centre, The University of Queensland, St. Lucia, Queensland 4072, Australia,³ Department of Disease and Stress Biology, The John Innes Centre, Norwich NR4 7UH, United Kingdom⁴

Received 3 October 2007/ Accepted 16 March 2008

Rhabdoviruses are important pathogens of humans, livestock, and plants that are often vectored by insects. Rhabdovirus particles have a characteristic bullet shape with a lipid envelope and surface-exposed transmembrane glycoproteins. Sigma virus (SIGMAV) is a member of the Rhabdoviridae and is a naturally occurring disease agent of Drosophila melanogaster. The infection is maintained in Drosophila populations through vertical transmission via germ cells. We report here the nature of the Drosophila innate immune response to SIGMAV infection as revealed by quantitative reverse transcription-PCR analysis of differentially expressed genes identified by microarray analysis. We have also compared and contrasted the immune response of the host with respect to two nonenveloped viruses, Drosophila C virus (DCV) and Drosophila X virus (DXV). We determined that SIGMAV infection upregulates expression of the peptidoglycan receptor protein genes PGRP-SB1 and PGRP-SD and the antimicrobial peptide (AMP) genes Diptericin-A, Attacin-A, Attacin-B, Cecropin-A1, and Drosocin. SIGMAV infection did not induce PGRP-SA and the AMP genes Drosomycin-B, Metchnikowin, and Defensin that are upregulated in DCV and/or DXV infections. Expression levels of the Toll and Imd signaling cascade genes are not significantly altered by SIGMAV infection. These results highlight shared and unique aspects of the Drosophila immune response to the three viruses and may shed light on the nature of the interaction with the host and the evolution of these associations.

Published ahead of print on 31 March 2008.

Present address: Department of Environmental Science, Policy, and Management, University of California, Berkeley, CA 94720.