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United States Department of Agriculture

Agricultural Research Service

Title: Highly pathogenic porcine reproductive and respiratory syndrome virus JXwn06 causes high mortality in vivo)

Author
item Kappes, Matthew
item Guo, Baoqing
item Lager, Kelly
item Henningson, Jamie
item Schlink, Sarah
item Miller, Laura
item Brockmeier, Susan
item Kehrli Jr, Marcus
item Yang, Han Chun
item Faaberg, Kay

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 5/11/2011
Publication Date: 6/4/2011
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.

Interpretive Summary:

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.

Last Modified: 05/24/2017
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