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Title: Pathogenesis of PCV2a and PCV2b virus in germ-free pigs

item Gauger, Phillip
item Lager, Kelly
item Baker, Amy
item Kehrli Jr, Marcus
item Cheung, Andrew

Submitted to: Pig Veterinary Society International Congress Proceedings
Publication Type: Proceedings
Publication Acceptance Date: 3/30/2008
Publication Date: 6/22/2008
Citation: Gauger, P.C., Lager, K.M., Vincent, A.L., Opriessnig, T., Kehrli, Jr., M.E., Cheung, A.K. 2008. Pathogenesis of PCV2a and PCV2b Virus in Germ-Free pigs. In: Proceedings of the International Pig Veterinary Society Congress, June 22-26, 2008, Durban, South Africa. Paper No. OR.01.28.

Interpretive Summary:

Technical Abstract: Genetic analysis of porcine circovirus type 2 (PCV2) reveals 2 subgroups that will be referred to as PCV2a and PCV2b representing the North American and European prototypes respectfully. This paper summarizes 3 studies comparing the pathogenesis of 2a and 2b viruses in germ-free pigs. In this PCV2-infection model there were 3 general outcomes following challenge. Outcome 1: Pigs became clinically abnormal and began to die acutely 21 dpi with peak mortality at 25-26 dpi. These pigs had significant alterations in their leukograms, very high virus loads (ave. 10.8 log10), and did not develop a humoral immune response. Outcome 2: Pigs that were clinically normal, had minor alterations in their leukograms much less virus load (ave. 5.3 log10), and had developed ELISA and VN antibody. Outcome 3: Pigs that were clinically normal, had moderately altered leukograms, high virus load (ave. 7.9 log10), and had not developed both ELISA and VN antibody. One limitation of this animal model is that pigs can only be maintained for about 6 weeks post challenge. At the conclusion of the experiment we assume the pigs in Outcome 2 would develop a protective immune response and survive. A protective immune response has been shown to be correlated with a decreased virus load in serum. It is not known if the pigs in Outcome 3 would eventually succumb to the viral infection or if they would develop a protective immunity. At this time, no known infectious cofactor has been identified in this study although clinical disease was reproducible and caused approximately 50% mortality, which is similar to previous studies involving an infectious cofactor and/or immune stimulation. Further study is necessary to assess whether other endogenous or exogenous cofactors are involved in the pathogenicity of PCV2a or PCV2b virus.