摘要
VC2002, isolated from postweaning multisystemic wasting syndrome(PMWS)-affected pig, is a mixture of two porcine circovirus genotype 2b(PCV2b) viruses, K2 and K39. Preliminary experiments disclosed short-term adverse effects of K39, but not K2, on porcine foetuses. These findings led to the hypothesis that infection of immuno-incompetent foetuses with K2 confers a status of immunotolerance, and postnatal super-infection with K39 triggers PMWS. To explore this hypothesis, nine 55-day-old foetuses were inoculated in utero(three with K2-104.3TCID50, three with K39-104.3TCID50 and three with medium), and foeto-pathogenicity examined. At 21 days post-inoculation(dpi), K2 did not induce pathology, whereas pathological effects of K39 were evident. Twenty-four 45-day-old foetuses were subsequently inoculated to examine the long-term effect of K2, including six with K2-high dose-104.3TCID50, six with K2-low dose-102.3TCID50 and 12 mock-inoculated controls. Both doses resulted in five mummified foetuses and one live-born piglet each(69dpi). K2 was recovered from all mummies. K2 and K2-specific antibodies were not detected in serum of the two live-born piglets at birth, indicating full control of K2 infection. The K2-low dose-infected piglet was immunostimulated at day 2, but not the K2-high dose-infected piglet. Both non-stimulated and stimulated K2-infected piglets were super-inoculated with K39 at day 6 or 8(taken as 0 days post super-inoculation). Low viral replication was observed in the non-stimulated K2-K39 piglet(up to 103.3 TCID50/g; identified as K39). In contrast, viral replication was extremely high in the stimulated K2-K39 piglet(up to 105.6TCID50/g) and identified as K2, indicating that K2 infection is controlled during foetal life, but emerges after birth upon immunostimulation. However, none of the piglets showed any signs of PMWS.
VC2002, isolated from postweaning multisystemic wasting syndrome（PMWS）-affected pig, is a mixture of two porcine circovirus genotype 2b（PCV2b） viruses, K2 and K39. Preliminary experiments disclosed short-term adverse effects of K39, but not K2, on porcine foetuses. These findings led to the hypothesis that infection of immuno-incompetent foetuses with K2 confers a status of immunotolerance, and postnatal super-infection with K39 triggers PMWS. To explore this hypothesis, nine 55-day-old foetuses were inoculated in utero（three with K2-104.3TCID50, three with K39-104.3TCID50 and three with medium）, and foeto-pathogenicity examined. At 21 days post-inoculation（dpi）, K2 did not induce pathology, whereas pathological effects of K39 were evident. Twenty-four 45-day-old foetuses were subsequently inoculated to examine the long-term effect of K2, including six with K2-high dose-104.3TCID50, six with K2-low dose-102.3TCID50 and 12 mock-inoculated controls. Both doses resulted in five mummified foetuses and one live-born piglet each（69dpi）. K2 was recovered from all mummies. K2 and K2-specific antibodies were not detected in serum of the two live-born piglets at birth, indicating full control of K2 infection. The K2-low dose-infected piglet was immunostimulated at day 2, but not the K2-high dose-infected piglet. Both non-stimulated and stimulated K2-infected piglets were super-inoculated with K39 at day 6 or 8（taken as 0 days post super-inoculation）. Low viral replication was observed in the non-stimulated K2-K39 piglet（up to 103.3 TCID50/g; identified as K39）. In contrast, viral replication was extremely high in the stimulated K2-K39 piglet（up to 105.6TCID50/g） and identified as K2, indicating that K2 infection is controlled during foetal life, but emerges after birth upon immunostimulation. However, none of the piglets showed any signs of PMWS.
