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Journal of Virology, June 2004, p. 5875-5882, Vol. 78, No. 11
0022-538X/04/$08.00+0 DOI: 10.1128/JVI.78.11.5875-5882.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
Department of Microbiology and Center for Salmon Disease Research, Oregon State University, Corvallis, Oregon 97330,1 Department of Biochemistry, Microbiology and Molecular Biology, University of Maine, Orono, Maine 04469,2 Department of Molecular Biology and Genetics, Cornell University, Ithaca, New York 14853,3 Hawaii Institute of Marine Biology, Kaneohe, Hawaii 967444
Received 13 October 2003/ Accepted 4 February 2004
Snakehead rhabdovirus (SHRV) affects warm-water fish in Southeast Asia and belongs to the genus Novirhabdovirus by virtue of its "nonvirion" (NV) gene. To examine the function of the NV gene, we used a recently developed reverse genetic system to produce a viable recombinant SHRV carrying an NV gene deletion. The recombinant virus was produced at the same rate and same final concentrations as the wild-type virus in cultured fish cells in spite of the NV gene deletion. The role of the NV protein in fish pathogenesis was also investigated. Zebra fish (Danio rerio) were infected with the NV deletion mutant or with a recombinant virus containing a copy of the SHRV genome, and similar mortality rates as well as final mortalities were recorded, suggesting no apparent role for the NV protein in fish pathogenesis. Interestingly, the unsuccessful rescue of fully viable recombinants with genomes containing deletions in the G/NV gene junction suggested a role for the gene junction in virus transcription and replication. Finally, we demonstrated that the SHRV glycoprotein can be replaced by the glycoprotein of infectious hematopoietic necrosis virus (IHNV) or by a hybrid protein composed of SHRV and IHNV sequences.
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