|Allende, R - UNIVERSITY OF NEBRASKA|
|Lu, Z - UNIVERSITY OF CONNECTICUT|
|Lewis, T - USDA/ARS/PIADC--DECEASED|
|Friesen, J - UNIVERSITY OF NEBRASKA|
|Galeota, J - UNIVERSITY OF NEBRASKA|
|Doster, A - UNIVERSITY OF NEBRASKA|
|Osorio, F - UNIVERSITY OF NEBRASKA|
Submitted to: Archives of Virology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: December 16, 1999
Publication Date: N/A
Interpretive Summary: Current vaccines for porcine reproductive and respiratory syndrome (PRRS) virus consist of live virus which has lost the ability to cause disease but retains the ability to grow and induce an immune response in swine. The purpose of this study was to determine the differences in genetic sequence between a virus that causes severe disease in swine and a vaccine strain of fPRRS virus. Genetic material of these viruses was 98% identical over the 15,374 base pair genome. Only four sequence differences which changed viral proteins were detected, 2 in non-structural proteins (Nsp1b and Nsp2) and 2 in structural proteins (ORF3 and ORF5). These changes may be responsible for the loss of disease causing ability in the vaccine virus.
Technical Abstract: Although live-attenuated vaccines have been used for sometime to control clinical symptoms of porcine reproductive and respiratory syndrome (PRRS) the molecular bases for the attenuated phenotype remain unclear. We had previously determined the genomic sequence of the pathogenic PRRS virus 16244B. Limited comparisons of structural protein coding sequence of an attenuated vaccine strain have shown 98% homology to the pathogenic 16244B Here we have confirmed the attenuated phenotype and determined the genomic sequence of that attenuated PRRS virus vaccine and compared it to 16244B isolate. Attenuated vaccine sequence was colinear with that of the strain 16244B sequence containing no gaps and 210 substitutions over 15,374 determined nucleotide sequence. We identified four amino acid changes distributed in Nsp1beta, Nsp2, ORF3 and ORF5. These changes may provide molecular bases for the observed attenuated phenotype.