|Blair, Carol - COLORADO STATE UNIV|
|Beaty, Barry - COLORADO STATE UNIV|
Submitted to: American Society for Virology Meeting
Publication Type: Abstract Only
Publication Acceptance Date: April 7, 2003
Publication Date: July 12, 2003
Citation: White, D.M., Wilson, W.C., Blair, C.D., Beaty, B.J. 2003. Possible overwintering mechanixm of bluetongue virus in the arthropod vector. Am. Soc. Virol. W49-1. 2003. Abstract. Interpretive Summary: Bluetongue virus (BTV) causes an economically important arboviral disease in U.S. livestock. BTV is maintained in nature by cycling between vertebrate animals (domestic and wild ruminants) and the main U.S. vector Culicoides sonorensis, a biting gnat. However, the mechanism by which the virus survives the winter when the insects are dormant has eluded researchers for many years. Persistent infection of the vector insect was demonstrated by the detection of several BTV gene sequences in larvae collected from the field very early in the transmission season (overwintering larvae), supporting the hypothesis that the virus overwinters inside it's insect vector. In addition, the detection of gene sequences necessary for the infection of insect cells in the absence of those necessary for the infection of animal cells suggests that BTV may not require abundant expression of the outer coat genes to persist in the insect vector. This could explain the low rate of isolation of virus from insects.
Technical Abstract: Bluetongue virus (BTV) causes an economically important arboviral disease in U.S. livestock. BTV is maintained in nature by cycling between vertebrate animals (domestic and wild ruminants) and the main U.S. vector Culicoides sonorensis. However, the overwintering mechanism of the virus has eluded researchers for many years. Embryonic culicoid cell lines and larval C. sonorensis collected from an endemic location in northern Colorado early in the transmission season were tested for the presence of BTV nucleic acid. Structural (L3, S7) and non-structural (S10) genes necessary for infection of insect cells were found in the absence of a structural gene (L2) necessary for vertebrate cell infection in all cell lines and roughly 10% of the field-collected culicoid pools. These data suggest that BTV may not require abundant expression of the outer coat genes to persist in the insect vector. This could also explain the low rate of isolation of virus from insects. If the vertebrate cell receptor ligand VP2 (encoded by L2) is absent or expressed at very low levels in the insect, traditional vertebrate cell-based isolation methods would be expected to be inefficient when used to examine insect-derived samples. Recovery of viral capacity to infect vertebrate cells could be linked to one of the many periods of significant metabolic change/activity in the life cycle of the insect (morphogenesis, blood feeding, etc.).