Pathogenicity and immune response against porcine circovirus type 3 infection in caesarean-derived, colostrum-deprived pigs

Abstract

Recently, a novel PCV species (PCV3) has been detected in cases associated with sow mortality, lesions consistent with porcine dermatitis and nephropathy syndrome, reproductive failure and multisystemic inflammation. The pathogenesis and clinical significance of PCV3 is still unclear. In this study, we investigated the immunopathogenesis of PCV3 in CD/CD pigs. Four treatment groups, PCV3 (n=6), PCV3-KLH (n=6), control (n=3) and control-KLH (n=3), were included with PCV3-positive tissue homogenate (gc=3.38×1012 ml−1 and gc=1.04×1011 ml−1), confirmed by quantitative PCR (qPCR) and next-generation sequencing. Clinical signs, viremia, viral shedding, systemic cytokines, humoral (IgG) and T-cellular response were evaluated for 42 days. At necropsy, tissues were collected for histological evaluation and PCV3 detection by qPCR and in situ hybridization. No significant clinical signs were observed through the study. Viremia was detected in both PCV3-inoculated groups from 3 days post-inoculation (p.i.) until the end of the study. Nasal shedding was detected from 3 to 28 days p.i. and faecal shedding was transient. PCV3 induced an early (7 days p.i.) and sustained (42 days p.i.) IgG response. No significant T-cell response was observed. Histological evaluation demonstrated lesions consistent with multisystemic inflammation and perivasculitis. All tissues evaluated were positive by qPCR and virus replication was confirmed by positive in situ hybridization. This study demonstrated the potential role of PCV3 in subclinical infection, producing a mild, multisystemic inflammatory response, prolonged viremia detectable for 42 days p.i., presence of IgG humoral response and viral shedding in nasal secretions. More research is required to understand and elucidate potential co-factors necessary in the manifestation and severity of clinical disease.

Porcine Circovirus 3 Detection in Aborted Fetuses and Stillborn Piglets from Swine Reproductive Failure Cases

“…There are also a significant number of bacterial pathogens that may account for reproductive disorders [ 2 ]. The three viruses studied here, apart from PCV-3, are already well recognized as putative causative agents of reproductive disease [ 36 , 37 , 38 , 39 ], and the results obtained in the present studies reinforce [ 4 , 20 , 40 ] the potential of PCV-3 as a pathogen able to cause reproductive problems, as suggested elsewhere [ 4 , 20 , 40 ]. The present study did not aim at establishing potential bacteria causing reproductive disorders; however, no lesions compatible with bacterial infections were observed during histologic evaluation in the studied tissues of fetuses and stillborn piglets.…”

“…40). These findings suggest a PCV-3 tropism mainly for vasculature, similar to what has been described in piglets with multisystemic inflammation [ 4 , 11 , 20 , 40 ]. Some of the animals from these latest reports also showed lesions compatible with porcine dermatitis nephropathy syndrome (PDNS) [ 4 , 11 , 12 ].…”

“…Two out of the six cases with high loads of PCV-3 in tissues showed a lack of histological lesions. These results are not surprising since other studies have already mentioned the lack of lesions even in the presence of great amounts of PCV-3 DNA [ 7 , 40 ]. A Hungarian group found high loads of PCV-3 in tissues from aborted and weak-born piglets with no gross lesions [ 6 ].…”

“…This animal was also positive to other pathogens such as PRRSV, Streptoccocus suis and Mycoplasma hyopneumoniae [ 8 ]. Additionally a recent experimental PCV-3 inoculation performed in the USA provided evidences that PCV-3 is able to produce multisystemic inflammation as well as subclinical infections [ 40 ]. Specifically, all animals of two different inoculated groups had prolonged viremia, but only 2/4 and 3/4 showed histopathologic lesions [ 40 ].…”

“…Additionally a recent experimental PCV-3 inoculation performed in the USA provided evidences that PCV-3 is able to produce multisystemic inflammation as well as subclinical infections [ 40 ]. Specifically, all animals of two different inoculated groups had prolonged viremia, but only 2/4 and 3/4 showed histopathologic lesions [ 40 ]. Thus, Temeeyasen et al [ 40 ] suggested that the PCV-3 pathogenesis is complex and of multifactorial nature.…”