Sows without the CD163 gene are not only resistant to porcine reproductive and respiratory syndrome (PRRS) virus, they also give birth to healthy, normal piglets — a finding that could ultimately lead to elimination of a devastating disease, researchers say.
In their study, the researchers demonstrated that the absence of CD163 in the sow is sufficient to protect the fetus from PRRS. Piglets from these sows may still be susceptible to the disease later in life, but they will respond better to PRRS virus vaccines, researchers from the University of Missouri and Kansas State University (KSU) said in Nature: Scientific Reports online in October 2017.1
CD163 as a receptor for the PRRS virus was first described in 2007. Previous studies by this same group of researchers showed that pigs with a complete knockout of the CD163 gene are free of PRRS virus infection.
The current study involved seven gilts with the CD163 knockout, which were bred with CD163-positive boars to produce CD163-free fetuses. The gilts were then challenged with PRRS virus strain NVSL 97-7895, reported Raymond “Bob” Rowland, PhD, of KSU, who led the research and presented findings at the 2017 North American PRRS Symposium.
Polymerase chain reaction data demonstrated that in sows with the CD163 gene, there’s a wide variation of virus concentration among fetuses, and they become infected at different times, Rowland said.
The reproductive form of the PRRS virus infection causes abortions, dead fetuses and respiratory disease in newborns. It can lead to 90% mortality of fetuses and neonates, along with increased sow mortality. Fetuses that survive the infection become continuous sources of the virus, resulting in endemically infected herds, he said.
Pork producers could save millions of dollars if pigs are protected from PRRS virus during the reproductive process, Rowland said at the symposium.
1 Rowland, RRR et al. Knockout of maternal CD163 protects fetuses from infection with porcine reproductive and respiratory syndrome virus (PRRSV). Nature, Scientific Reports 7, Article number: 13371(2017). doi:10.1038/s41598-017-13794-2.