Tissue tropisms of porcine parvovirus in swine

Abstract

Late-term gestation swine fetuses, similar to adult animals, are able to effectively mount immune response and survive porcine parvovirus (PPV) infection. An exception to this is the Kresse strain of PPV, which causes fetal death in late-term gestation swine fetuses. In an effort to understand the basis for this profound difference in pathogenicity between Kresse strain and the prototype strain of PPV, NADL-8, studies were designed to examine potential difference in sites of replication and quantity of virus produced between Kresse and NADL-8 strains. In order to define the sites of viral replication or sites of viral sequestration in situ hybridization, using digoxigenin-labeled strand-specific oligonucleotide probes, was applied to detect the presence of either double stranded viral DNA (RF) or viral single stranded DNA in tissues of infected fetuses. The presence and the state of viral DNA was confirmed by Southern blot hybridization. Relative amounts of RF-DNA synthesis in each tissue was compared between the two virus strains. Virus replication appeared to be of comparable levels in the livers of both NADL-8 and Kresse infected swine fetuses. Differences between these strains were observed in the brain and spleen; RF-DNA was detected in the brain and spleens of Kresse infected fetuses but not in NADL-8 infected ones. These findings indicate that differences in DNA replication of the PPV strains in selective sites, as well as the quantity of virus produced, may explain the distinction in pathogenesis of these viruses.

Coinfection by Porcine Circoviruses and Porcine Parvovirus in Pigs with Naturally Acquired Postweaning Multisystemic Wasting Syndrome

“…PPV also has extralymphoid targets, including pulmonary and renal epithelium, hepatocytes, and endothelium. 21 Although controversial, it has been proposed on the basis of in vitro and in vivo studies that observed differences in virulence among PPV isolates may relate to differences in tissue tropism. 6,16 Although similar studies have yet to be performed with PCV isolates, it appears, on the basis of immunohistochemical analyses of lesions in naturally and experimentally infected pigs, [1][2][3]10,12 that, compared with PCV 1, the recent isolates of PCV 2 have a wider tropism than just lymphoid tissue, which may account, in part, for its virulence in vivo.…”

“…Pigs with PMWS generally present with clinical signs and corresponding lesions at an age when maternal antibodies would be waning. 21 Pigs exposed to PPV at this time could be subclinically infected and transiently viremic prior to the development of immunity. 18 Although the pathogenesis of the newly described strains of PCV is not currently known, a similar scenario could also occur after infection of postweaning age pigs with this virus.…”

Molecular basis for porcine parvovirus detection in dead fetuses

“…Tissue tropism of PPV, replication in selective sites and quantity of virus produced may explain the distinction in pathogenesis. Viral antigen and viral DNA replication in the brain were demonstrated only in late-term fetal infection with the Kresse strain (Choi et al, 1987;Oraveerakul et al, 1993). In the present study, the replicative form of PPV genome was not demonstrated in tissue samples and PPV was not investigated in nervous tissue, but the viral genome was detected in many tissues, showing evidence of PPV spreading and tissue damage in transplacentally infected fetuses from vaccinated sows.…”

“…Differences in pathogenicity between PPV NADL-8 and Kresse strains in late-term gestation have been described, indicating the Kresse strain as more virulent (Choi et al, 1987;Oraveerakul et al, 1993). Comparing relative virulence of the same two prototype strains in experimentally infected porcine fetuses at immune competence age showed that the NADL-8 strain causes more fetal mortality (Lager et al, 1992).…”

Simultaneous Detection of Porcine Circovirus 2 and Porcine Parvovirus in Naturally and Experimentally Coinfected Pigs by Double in Situ Hybridization

“…PPV is not regarded as a significant cause of mortality in postweaning and growing pigs, although PPV has an in vivo tropism for monocytes and lymphocytes. 3,18 PCV2 virion production in vivo is upregulated as a result of immune stimulation. 15 Because both PCV2 and PPV are DNA viruses and depend upon cellular DNA synthesis for optimal virion production, stimulation of host DNA synthesis by PPV could inadvertently promote PCV2 replication.…”