Submitted to: American Veterinary Medical Association Abstract
Publication Type: Abstract Only
Publication Acceptance Date: May 1, 2013
Publication Date: July 19, 2013
Citation: Brockmeier, S. 2013. Pathogenesis of highly-pathogenic Asian PRRSV in pigs. 2013 American Veterinary Medical Association (AVMA) Annual Convention, July 19-23, 2013, Chicago, Illinois. Paper No. 13917. Technical Abstract: In 2006, Chinese investigators reported a unique syndrome in growing swine that was highlighted by clinical signs of high fever, anorexia, listlessness, red discoloration of skin, respiratory distress and very high morbidity and mortality rates. Originally known as porcine high fever disease (PHFD), this syndrome quickly spread to Vietnam and other Southeast Asian countries. Concern existed that PHFD was caused by a new disease agent, however, extensive diagnostic testing only revealed known pathogens. One consistent finding was detection of porcine reproductive and respiratory syndrome virus (PRRSV) with two discontinuous deletions in the replicase polyprotein known as nonstructural protein 2, and two single nucleotide deletions in the 5' and 3' untranslated regions. Experimental infection of swine with virus derived from an infectious clone of the Chinese JX143 PRRSV isolate confirmed that this virus was the causal agent leading to this lineage of virus being called highly pathogenic PRRSV (HP-PRRSV). Due to the severity of PHFD, there was still speculation that some unique factor may predispose Asian pigs to this disease, e.g., husbandry practices, endemic infections with other pathogens, climate, or host genetics. Although a number of studies have associated genetic changes in PRRSV with an attenuation phenotype, there appears to be no single locus for which mutations confer a predictable change in virulence. Collectively, this suggests the factors that contribute to PRRSV pathogenicity are complex and viral strain-specific. To investigate the pathogenesis of HP-PRRSV in swine, and the potential contribution of host genetics and husbandry practices to the pathogenicity of HP-PRRSV in U.S. swine, we compared the pathogenicity of a virus derived from an infectious clone from China to that of a North American prototype strain in pigs of various ages. We found that HP-PRRSV caused a severe high mortality disease, the virus replicated at a 100X higher rate in pigs than the North American prototype strain, and HP-PRRSV induced a novel systemic cytokine release syndrome associated with severe clinical disease. Vaccination with a commercially available U.S. vaccine attenuated the clinical effect of the HP-PRRSV challenge when compared to non-vaccinated challenge controls. However, many of the vaccinated pigs became very sick following challenge but were recovering by the conclusion of the experiment. Asian HP-PRRSV strains inducing this severe disease syndrome pose a serious threat to the U.S. swine industry.