Interactions of porcine circovirus type 2 and porcine reproductive and respiratory syndrome virus

Porcine circovirus associated disease (PCVAD) has made an economic impact in global swine production, is caused by porcine circovirus type 2 (PCV2) and manifests in forms of multisystemic disease, wasting, pneumonia, diarrhea in growing pigs and reproductive failure in gilts and sows. PCVAD is enhanced by PRRSV co-infection alongside PCV2 infection in pigs and is not very well understood except that PRRSV potentiates PCV2 replication in the host. We characterized apoptosis in gnotobiotic pigs caused by both PCV2a and PCV2b and for the first time established that both PCV2a and PCV2b are able to promote cell death in the hepatocytes of gnotobiotes of clinically affected pigs leading to hepatic failure. We further delineated the role of PRRSV in affecting PCV2a and PCV2b apoptosis in specific pathogen free (SPF) pigs and demonstrated that PRRSV does not cause apoptosis induction in PCV2a and PCV2b infected pigs. We compared and demonstrated that in vitro differences in PCV2 or PRRSV replication or IFN gamma; and IL-10 release in porcine alveolar macrophages (PAMs) inoculated with several PCV2-PRRSV combinations are small and not dependent on ORF1 or ORF2 origin. We analyzed the shedding of both PCV2a and PCV2b in piglets co-infected with PRRSV and ascertained that PRRSV is capable of prolonging PCV2 viremia and subsequent shedding in the nasal, oral secretions and fecal excretion that can increase horizontal transmission of PCV2a and PCV2b in nayve herds. Finally we also verified if prior PRRSV exposure had any detrimental effect on PCV2 vaccines currently available in the US market. We were able to establish that the PCV2 vaccines are able to provide protective immunity to piglets that had prior PRRSV infection.