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Title: UPDATE ON BLUETONGUE VIRUS PERSISTENCE IN CULICOIDES SONORENSIS

Author
item Wilson, William - Bill
item Drolet, Barbara
item Mecham, James

Submitted to: United States Animal Health Association Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: 7/20/2005
Publication Date: 11/8/2005
Citation: Wilson, W.C., Drolet, B.S., Mecham, J.O. 2005. Update on bluetongue virus persistence in Culicoides sonorensis. United States Animal Health Association Proceedings, 109th Annual Meeting.

Interpretive Summary: The insect-transmitted bluetongue virus causes disease in cattle, sheep, and wild ruminants and it presence in the U.S. results in significant economic losses due to trade restrictions. A biting midge or gnat transmits this virus from animal to animal. This manuscript describes a non-infectious persistent bluetongue virus in the vector insect. This finding may be significance in understand the maintenance of this virus in nature.

Technical Abstract: A persistent bluetongue virus (BTV) infection was investigated in a cell line (KC) derived from the North American insect vector of BTV, Culicoides sonorensis. Inoculation of the KC cell line with BTV resulted in a productive noncytopathic, persistent infection in which viral titers diminished over time. The uninoculated KC cell line itself was found to contained 8 of 10 BTV gene segments, lacking 2 and 5 that encode the outer coat proteins and did not produce virus particles infectious for mammalian cells. This non productive infection is referred to as a host specific persistent (HSP) virus, as it was found only in the insect cells. A silent mutation in segment 3 that encodes an inner core protein was used to trace the HSP virus back through more than a hundred passages of the KC cell line. Segments 3 and 10 of the HSP virus had sequence homology with BTV serotype 17. Antigenic proteins of the HSP virus were detected by immunohistochemistry with various anti BTV sera. Attempts to rescue the HSP virus by superinfection of the mammalian cell culture were unsuccessful. Our results suggest that the HSP virus is defective or down-regulated in the ability of infected cells to produce the outer coat proteins necessary for infectivity in mammalian cells.