|Bernard, K - U OF WISCONSIN - MADISON|
|Israel, B. - U 0F WISCONSIN - MADISON|
Submitted to: Intervirology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: June 1, 1997
Publication Date: N/A
Interpretive Summary: Bluetongue virus (BTV) causes disease in cattle and sheep. There are five immunologic types or serotypes of BTV in the US but there are avirulent and virulent strains within these serotypes. This report genetically characterizes a avirulent and a virulent strain of BTV type 17. Three regions of the gene encoding for an outer coat protein were variable and may account for the differences in virulence. It is known that BTV can exchange genome segments between serotypes. This is called reassortment and is thought to be a relatively rare event in nature. This report establishes a naturally reassortment between BTV type 17 and type 10. This is the first report of a potential virulence marker (i.e. a specific protein sequence that could be associated with virulence).
Technical Abstract: Genome Segments 2 & 3 were completely sequenced for one virulent and one avirulent bluetongue virus serotype 17 (BLU -17). These two segments were previously shown to be virulence associated markers. The marker on segment 2 was characterized by a change in the neutralization domain on its protein product, VP2. The nucleotide sequences for segment 2 were 94.5% identical, & their predicted proteins differed by 34 amino acids or 3.7%. Three clusters of variability were identified which may be involved with viral neutralization. Due to the diversity of the natural isolates, we were unable to determine which mutations affected the virulence associated neutralization domain. The marker on segment 3 was characterized by a mobility shift in polyacrylamide gel electrophoreses (PAGE). The nucleotide sequences were 95.0% identical & their predicted proteins differed by four amino acids or 0.4%, hence amino acid changes were relatively conserved; therefore, they are not likely responsible for virulence. The segment 3 sequences were compared to published sequences and evidence was found to suggest that the virulent isolate was the result of natural reassortment between a BLU- 17 and BLU-10 isolate.