Biology of Porcine Parvovirus (Ungulate parvovirus 1)

Abstract

Porcine parvovirus (PPV) is among the most important infectious agents causing infertility in pigs. Until recently, it was thought that the virus had low genetic variance, and that prevention of its harmful effect on pig fertility could be well-controlled by vaccination. However, at the beginning of the third millennium, field observations raised concerns about the effectiveness of the available vaccines against newly emerging strains. Subsequent investigations radically changed our view on the evolution and immunology of PPV, revealing that the virus is much more diverse than it was earlier anticipated, and that some of the "new" highly virulent isolates cannot be neutralized effectively by antisera raised against "old" PPV vaccine strains. These findings revitalized PPV research that led to significant advancements in the understanding of early and late viral processes during PPV infection. Our review summarizes the recent results of PPV research and aims to give a comprehensive update on the present understanding of PPV biology.

Keywords: VP2 trimer; genetic diversity; mutation rate; nuclear localization signal; porcine circovirus type 2; ungulate protoparvovirus 1; viral entry.

Figure 1

Major time points of Porcine Parvovirus (PPV) infection and immune response. The maternal antibodies protect the piglets passively (green line) until 9–22 weeks of age. The animals should be inoculated first after the depletion of maternal antibodies, and long-term immunity is maintained by booster vaccination. The embryos are susceptible to the infection (red line) until the Development of immune competence around day 70 day of gestation (green line). The consequences of the intrauterine infection depend on the time of the infection.

Figure 2

Amino acid residues with known function on the surface of a capsid protein 2 (VP2) trimer of PPV. A–C outer surface is shown. (A) amino acid (aa) 348 highlighted contributing to P2 replication in the canine cell line A72; (B) aa 378 and 383 are involved in tissue tropism and probably in virulence; (C) aa 228E, 419Q and 436T are characteristic of the members of the D cluster; (D) aa K272, K275, K487 and R576 form a nuclear localization motif on the inner surface of the trimer. Numbering is presented according to NADL-2 VP2 sequence, amino acid changes labeled by commonly used colloquial nomenclature. Trimer was generated by Viper program and visualized by Polivew.