Submitted to: Porcine Reproductive and Respiratory Syndrome International Symposium
Publication Type: Abstract only
Publication Acceptance Date: 10/15/2007
Publication Date: 11/30/2007
Citation: Wang, Y., Liang, Y., Han, J., Burhardt, K.M., Vaughn, E.M., Roof, M.B., Faaberg, K.S. 2007. Attenuation of PRRSV by chimera construction [abstract]. International Porcine Reproductive and Respiratory Syndrome (PRRS) Symposium. Paper No. 29. Interpretive Summary:
Technical Abstract: Two genetically distinct infectious recombinant virus clones (pMLV, constructed from Ingelvac® PRRS MLV and pMN184, constructed from virulent strain MN184) were developed to study attenuation of contemporary PRRSV. Two reciprocal chimeric clones (pMLVORF1/MN184 and pMN184ORF1/MLV) were then constructed. In vitro studies demonstrated that the rescued chimeric viruses possessed intermediate growth properties compared to recombinant rMLV and rMN184. Swine inoculation with rMN184 and rMLV verified that these viruses fully mimicked the respective parent virus. Earlier and higher antibody responses were detected in animals infected with rMN184 and the chimeras in contrast to those infected with rMLV. However, chimeric virus treatment groups showed much less severe pathogenesis when compared to the rMN184 group. These data suggested that genetic aspects of Ingelvac® PRRS MLV 5’ UTR/ORF1 replicase region and/or the structural proteins/3’ UTR can serve to attenuate virulent strain MN184. The data also indicated that designer PRRSV vaccines could be developed, keeping the known 5’ UTR/replicase region of an early vaccine strain such as Ingelvac® PRRS MLV intact, but replacing the structural protein/3’ UTR domain with that of an emerging virulent virus. The recent “fatal” Chinese isolates may represent one emerging virus genotype. The largest nsp2 deletion (87 bases) noted in these newest strains encompass the second largest of three discontinuous deletions previously described in virulent strain MN184. However, the Chinese isolates are still more similar to the RFLP142 genomes (~ 94% ORF5 nucleotide identity). Other novel amino acid islands were seen throughout the ORF1 polyprotein (particularly nsp1beta and nsp2) and in structural proteins GP2, GP3, GP5 and N. A one base deletion in the 3’ UTR was also noted. A rapid vaccine for these isolates may be completed by the exchange of the ORF1 region with that of a recombinant attenuated strain.