Mortality in pigs given PCV2 virus derived from DNA clones

Authors: Lager, Kelly; Gauger, Phillip; Baker, Amy; OPRIESSNIG, TANJA - IOWA STATE UNIVERSITY; Kehrli Jr, Marcus; Cheung, Andrew

Submitted to: Veterinary Record
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 6/5/2007
Publication Date: 9/22/2007
Citation: Lager, K.M., Gauger, P.C., Vincent, A.L., Opriessnig, T., Kehrli, Jr., M.E., Cheung, A.K. 2007. Mortality in pigs given porcine circovirus type 2 subgroup 1 and 2 viruses derived from DNA clones. Veterinary Record. 161(12):428-429.

Interpretive Summary: The clinical presentation following infection with porcine circovirus type 2 (PCV2) ranges from sub-clinical to one of several disease states known collectively as porcine circovirus diseases (PCVD). In 2005 a disease spread rapidly through finishing barns in the U. S. that was recognized as an acute onset of high mortality. Investigations into these cases consistently recovered PCV2 and this syndrome was associated with PCVD. Genetic analysis revealed the isolates belong to PCV2 group 1, a subgroup that had not previously been recognized in the United States. Subgroup 2 has been in the U.S. since the mid 1990s. All 4 pigs that received the group 1 virus were severely affected 22-27 days-post-infection (dpi) and 1 of the 4 pigs given group 2 virus was severely affected by 35 dpi, the end of the experiment. This communication is the first report of inoculation of germ-free pigs with virus derived from infectious DNA clones constructed from subgroup 1 and 2 isolates recovered from affected swine in North Carolina. The clinical effects observed in this study are comparable to experiments in which germ-free pigs infected with PCV2 group 2 virus received an immune-stimulation event (co-infection with porcine parvovirus or injection with adjuvant). Those pigs manifested severe disease with distinctive lesions. The conclusion of those studies was that a co-factor was needed to induce disease since pigs infected only with PCV2 did not develop disease. The presence of severe disease in pigs in which we could not detect any co-factor suggests one of three things: 1) there is an unidentified exogenous factor that acted in synergy with the PCV2 infection; 2) there is an unknown endogenous factor that behaved similarly, or 3) PCV2 infection with virus derived from a DNA clone was capable of inducing severe disease without a co-factor.

Technical Abstract: The clinical presentation following infection with porcine circovirus type 2 (PCV2) ranges from sub-clinical to one of several disease states known collectively as porcine circovirus diseases (PCVD). In 2005 a disease spread rapidly through finishing barns in the U. S. that was recognized as an acute onset of high mortality. Investigations into these cases consistently recovered PCV2 and this syndrome was associated with PCVD. Genetic analysis revealed the isolates belong to PCV2 group 1, a subgroup that had not previously been recognized in the United States. Subgroup 2 has been in the U.S. since the mid 1990s. All 4 pigs that received the group 1 virus were severely affected 22-27 days-post-infection (dpi) and 1 of the 4 pigs given group 2 virus was severely affected by 35 dpi, the end of the experiment. This communication is the first report of inoculation of germ-free pigs with virus derived from infectious DNA clones constructed from subgroup 1 and 2 isolates recovered from affected swine in North Carolina. The lesions and clinical effects observed in this study are comparable to experiments in which germ-free pigs infected with PCV2 group 2 virus received an immune-stimulation event (co-infection with porcine parvovirus or injection with adjuvant). Those pigs manifested severe disease with distinctive lesions. The conclusion of those studies was that a co-factor was needed to induce disease since pigs infected only with PCV2 did not develop disease. The presence of severe disease in pigs in which we could not detect any co-factor suggests one of three things: 1) there is an unidentified exogenous factor that acted in synergy with the PCV2 infection; 2) there is an unknown endogenous factor that behaved similarly, or 3) PCV2 infection with virus derived from a DNA clone was capable of inducing severe disease without a co-factor.