ARS | Publication request: Highly pathogenic porcine reproductive and respiratory syndrome virus JXwn06 causes high mortality in vivo

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: May 11, 2011
Publication Date: June 4, 2011
Citation: Kappes, M.A., Guo, B., Lager, K.M., Henningson, J.N., Schlink, S.N., Miller, L.C., Brockmeier, S., Kehrli, Jr., M.E., Yang, H., Faaberg, K.S. 2011. Highly pathogenic porcine reproductive and respiratory syndrome virus JXwn06 causes high mortality in vivo [abstract]. XIIth International Nidovirus Symposium. p. 80.

Technical Abstract: In 2006, a large-scale outbreak of highly pathogenic atypical porcine reproductive and respiratory syndrome virus (PRRSV) spread throughout the swine population in China. Causative PRRSV isolates were characterized genetically by a unique 30aa deletion in PRRSV nonstructural protein 2 and clinically by high fever, morbidity and mortality. In this study using US high-health swine, Chinese Type 2 PRRSV outbreak strain rJXwn06 was assessed on parameters of disease, viral growth, and cytokine expression in relation to the prototypic Type 2 strain VR-2332. JXwn06 challenge resulted in overt clinical signs of disease, a 33% mortality rate, reduction in weight gain, and an increase in lung lesions, thymus atrophy, pulmonary bacterial load, and lymph adenopathy as compared to VR-2332. Viral isolation and qPCR data both indicated JXwn06 infected pigs maintained viral titers (TCID50) 2-3 log10 higher and 1-2 log10 higher copy numbers of PRRSV RNA as compared to VR-2332. Cytokine assays showed VR-2332 serum cytokine protein levels were similar to the control group throughout the study. Unlike VR-2332, JXwn06 challenge group showed transient elevation of IL-1, IFN-, TNF-alpha, and IL-2 protein levels at the later time points as compared to VR-2332 and negative control groups. The JXwn06 contact group had elevated IL-1beta, IL-2, IL-4, IL-10, IL-12, and IFN-gamma in response to infection. It is believed the differences between JXwn06 groups may be attributed to transmission of the most fit viruses to the contact group by a natural route of infection. Importantly, JXwn06 contacts both upregulated anti-inflammatory IL-10 and transiently downregulated TNF-alpha, positive and negative regulators of the critical PRRSV receptor CD163 respectively. These results point to a possible mechanism of CD163 upregulation in vivo by JXwn06 that may aid in growth kinetics and virulence.