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ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Virus and Prion Research » Research » Publications at this Location » Publication #266898
Title: HP-PRRSV challenge of 4 and 10-week-old pigs

Author
item Lager, Kelly
item Faaberg, Kay
item GUO, BAOQING - Iowa State University
item Brockmeier, Susan
item Henningson, Jamie
item Schlink, Sarah
item Miller, Laura
item Kappes, Matthew
item Kehrli Jr, Marcus
item Loving, Crystal
item Nicholson, Tracy
item YANG, H - China Agricultural University

Submitted to: Meeting Proceedings
Publication Type: Proceedings
Publication Acceptance Date: 4/22/2011
Publication Date: 5/10/2011
Citation: Lager, K.M., Faaberg, K.S., Guo, B., Brockmeier, S., Henningson, J.N., Schlink, S.N., Miller, L.C., Kappes, M.A., Kehrli, Jr., M.E., Loving, C.L., Nicholson, T.L., Yang, H.C. 2011. HP-PRRSV challenge of 4 and 10-week-old pigs. In: Proceedings of the 5th Asian PRRSpective Symposium, May 10, 2011, Bangkok, Thailand. 6 pages.

Interpretive Summary:

Technical Abstract: In 2006 a unique syndrome was recognized in growing pigs in China with the predominant clinical signs being high fever, anorexia, listlessness, red discoloration of skin, and respiratory distress. The disease had a very high morbidity and mortality rate and became known as porcine high fever disease. Although there was a great concern this syndrome may have been caused by a new pathogen, extensive diagnostic testing only revealed known pathogens. One consistent finding in affected pigs was the detection of porcine reproductive and respiratory syndrome virus (PRRSV) that had unique genetic mutations in the nsp2 gene. This led to the suspicion that PRRSV was the primary cause of porcine high fever disease, an assumption confirmed later by several experiments. Experimental infection of pigs by Zhou, et al., and Tian., et al, reproduced the clinical disease providing strong evidence for the role of PRRSV as the causal agent of porcine high fever disease. However, there was still a question if there was some unknown agent in the PRRSV preparations that increased the severity of the clinical disease over what was expected for a "routine" PRRSV infection. This question was put to rest by Lv et al., when porcine high fever disease was reproduced with virus derived from an infectious clone of the JX143 PRRSV isolate. These studies demonstrated that PRRSV isolates with a common genetic motif had a causal role in porcine high fever disease leading to this lineage of virus being called highly pathogenic PRRSV (HP-PRRSV). In the United States the swine industry has closely followed the porcine high fever disease story. In our laboratory we developed a collaboration with Dr. Yang, China Agricultural University, Beijing, China to import the plasmid containing a full-length clone of the JXwn06 HP-PRRSV isolate. Infectious virus (rJXwn06) was rescued from the clone and used to inoculate young pigs in a series of studies that were recently completed. The clinical results will be summarized in this proceeding and additional data will be presented at the meeting. The first experiment compared the pathogenicity of the rJXwn06 HP-PRRSV with the North American prototype PRRSV, VR-2332, in 4-week-old pigs. Fifty-five conventionally-raised pigs weaned at 3 weeks of age were randomly divided into one of 5 groups (11 pigs per group) that received the following treatments: Group 1 - a sham intranasal inoculation; Group 2 - a "low" dose intranasal challenge with the rJXwn06 virus; Group 3 - a "high" dose intranasal challenge with the rJXwn06 virus; Group 4 - a low dose intranasal challenge with the VR-2332 virus, and Group 5 - a high dose intranasal challenge with the VR-2332 virus. Both challenge viruses had been propagated in MARC-145 cell cultures and each virus was diluted to 1 x 10** CCID50/mL concentration for the high dose. The low dose challenge virus had a concentration of 1 x 10** CCID50/mL. In experiments 2 and 3, all virus challenges consisted of the "high" dose. All inoculations consisted of a 2 ml volume (either sham or virus) given intranasally. Pigs were bled on days 0, 4, 7, 11, and 14 days-post-inoculation (dpi). Pigs were scheduled for necropsy at 14 dpi. Pigs were weighed -1, 7, 14 dpi. The second experiment compared the pathogenicity of the rJXwn06 and VR-2332 viruses in 10-week-old pigs. Thirty-two pigs were divided into 4 treatment groups: Group 1 was sham inoculated controls (n = 8); Group 2 - high dose challenge rJXwn06 virus (n=12); Group 3 was 4 contact pigs that were co-mingled with the Group 2 pigs at 2 dpi and housed together until 13 dpi, the end of the study; and Group 4 - high dose VR-2332 challenge (n = 8). Pigs were bled on 0, 4, 7, 11 and 13 dpi and weighed on -1, 7, and 13 dpi. The third experiment tested the efficacy of a commercially available modified-live vaccine (Inglevac PRRSV MLV, Boehringer Ingelheim, Ve