Modification of PCV-2 virulence by substitution of the genogroup motif of the capsid protein

Allemandou, Aude; Grasland, Béatrice; Hernandez-Nignol, Anne-Cécile; Kéranflec'h, André; Cariolet, Roland; Jestin, André

2C 2D isolates were noted on pigs inoculated at the age of eight months without immunostimulation. Moreover, PMWS was reproduced in SPF piglets with the same PCV-2b isolate using the virus without immunostimulation [29] . We also previously demonstrated that a PCV-2b infectious clone (the same isolate as in this study) was infectious in vivo and was able to trigger clinical PMWS in an SPF piglet when PCV-2b clone transfection and immunostimulation were combined [21] . In this previous work, the PCV-2b genomic load found in the lymphoid tissues of the PMWS-affected piglet reached an average of 10 14 genome copies/g of tissue at 32 dpt. In our present study, the maximum genomic load in organs was 10 10.6 genome copies/g of tissue at 35 dpt in a pig inoculated with the PCV-2b clone which is below the PMWS diagnosis threshold of 10 11 genome copies/g of tissue proposed by Blanchard et al. [24] . The differences found between these two studies could be explained by the quantity of DNA injected in pigs. In contrast, the PCV-2a infectious clone was not previously tested for virulence itself, although the virus failed to induce PMWS in piglets, while it was recovered from a diseased piglet [20] . Thus the two parental clones PCV-2a and PCV-2b showed differences in experimental conditions similar to the infectious virus.