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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. The hypothesis to be tested was that the presence of the CD163 knockout genotype (CD163 KO) of the dam would be sufficient to protect fetuses following maternal infection with PRRSV. CD163 is the receptor for the virus.
The results from this study clearly demonstrate that the absence of CD163 in the dam is sufficient to protect the PRRSV-susceptible fetus. Although CD163-positive offspring derived from CD163 KO dams are susceptible to virus immediately after birth, the protection from PRRSV in utero provides a means to eliminate a major source of economic loss and animal suffering.
The results demonstrate a practical means to eliminate PRRSV-associated reproductive disease, a major source of economic hardship to agriculture.
Randall S. Prather, Kevin D. Wells, Kristin M. Whitworth, Maureen A. Kerrigan, Melissa S. Samuel, Alan Mileham, Luca N. Popescu & Raymond R. R. Rowland. Knockout of maternal CD163 protects fetuses from infection with porcine reproductive and respiratory syndrome virus (PRRSV). Scientific Reports 7, Article number: 13371 (2017) doi:10.1038/s41598-017-13794-2
