Knockout of maternal CD163 protects fetuses from infection with porcine reproductive and respiratory syndrome virus (PRRSV)

Sci Rep. 2017 Oct 17;7(1):13371. doi: 10.1038/s41598-017-13794-2.

Abstract

After infection of the porcine dam at about 90 days of gestation, porcine reproductive and respiratory syndrome virus (PRRSV) crosses the placenta and begins to infect fetuses. Outcomes of include abortion, fetal death and respiratory disease in newborn piglets. CD163 is the receptor for the virus. In this study, CD163-positive fetuses, recovered between 109 days of gestation or 20 days after maternal infection, were completely protected from PRRSV in dams possessing a complete knockout of the CD163 receptor. The results demonstrate a practical means to eliminate PRRSV-associated reproductive disease, a major source of economic hardship to agriculture.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alleles
  • Animals
  • Antigens, CD / genetics*
  • Antigens, CD / metabolism
  • Antigens, Differentiation, Myelomonocytic / genetics*
  • Antigens, Differentiation, Myelomonocytic / metabolism
  • Gene Knockout Techniques
  • Genotype
  • Host-Pathogen Interactions / genetics*
  • Porcine Reproductive and Respiratory Syndrome / genetics*
  • Porcine Reproductive and Respiratory Syndrome / virology*
  • Porcine respiratory and reproductive syndrome virus / physiology*
  • Receptors, Cell Surface / genetics*
  • Receptors, Cell Surface / metabolism
  • Swine

Substances

  • Antigens, CD
  • Antigens, Differentiation, Myelomonocytic
  • CD163 antigen
  • Receptors, Cell Surface