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Reproductive PRRS accounts for 45% of losses in U.S. swine herds. Using CRISPR/Cas9 technology to knockout the maternal CD163, researchers can create a protective shell around that fetus and produce a healthier pig.
December 4, 2017
The sows or gilts are bred, the pregnancies confirmed. The plan was executed. The time, money, effort and all resources invested in a well-planned, managed breeding program. Then it happens. Sows or gilts start aborting litters and you soon find yourself weaning 30 pigs from 26 sows in one farrowing room. The remaining 200 expected piglets were either aborted, stillborn or mummified. For those piglets that do survive, you wonder if they will even make it to the finishing barn, plagued with respiratory problems. This frustrating cycle continues room after room, gestation cycle after cycle.
Unfortunately, this scenario happens in real pig farming too often. Most pig caretakers can give you vivid details of the worse breeding cycles in the barn.
Porcine reproductive and respiratory syndrome is the most economically and emotionally draining disease in the North America, Europe and Asian swine industries. In North America alone, PRRS costs producers approximately $600 million annually.
The PRRS virus can attack the swine herd in two ways: a respiratory form that weakens young pigs’ ability to breathe and a more severe reproductive form that causes mass deaths in pigs during late-pregnancy. Losses are the result of respiratory disease in young pigs, poor growth performance, reproductive failure and in utero infection.
“Reproductive PRRS alone accounts for estimated 45% of losses or in its severest form can result in 90% mortality of fetuses/neonates, along with increased mortality for the dams,” explains Raymond “Bob” Rowland, Ph.D., Kansas State University researcher.
Although farms take strict measures to protect the herd from PRRS, it rears its ugly head over and over again. Research from the University of Minnesota shows PRRS remains in the environment up to 14 weeks, and 58% of the farms will break again.
Since PRRS introduction to North America in 1987, the industry searches for a solution to eliminate the disease. However, currently, the strategy for PRRS is about control or managing it. Only a few farms carry the PRRS-negative status. The remaining operations wait for the next outbreak while research teams tackle the problem, seeking scientific solutions.
Knocking out PRRS seemed like impossible a mission until 2015 when the development of a PRRS-resistant pig was introduced by Randall Prather and the University of Missouri research team. The swine industry soon learned that CD163 protein is the receptor for the virus. Using CRISPR/Cas9 technology, the CD163 protein was removed successfully from pigs by the research team.
Still, the PRRS-resistant pigs need to be tested in the barns. A job that Rowland and his team were designed to do, given the technology utility. “Good illustration of not only the power of technology but the power of collaboration,” Rowland tells National Hog Farmer.
Today, PRRS-resistant pigs are not found on America’s pig farms, however, it is now possible after regulatory hurdles are conquered. Still, Rowland and his collaborators think toward the future, continuing asking the tough PRRS questions and helping the industry to end the PRRS battle.
At the North American PRRS Symposium, Rowland debuted the next leg in the knockout PRRS research — ending reproductive PRRS. Stopping the virus from transferring in the uterus will eliminate the massive deaths of pigs in late-pregnancy. “When we look at ways to control this disease, it really begins with reproduction. We want to keep this disease out of the reproductive process, and we have found a way to do that,” says Rowland.
By genetic design, all proteins serve a purpose, and the CD163 protein is no different, however removing it protects the pigs from PRRS. According to Rowland, CD163 removes hemoglobin from the blood. In humans over time hemoglobin can build up and become toxic. Rowland and research teams prove that pigs can exist healthy without CD163 due to their shorter live span.
In spite of this, a better solution is to use the technology to produce a pig with normal CD163 function. A way to do it is to focus on the reproduction stage and protect fetuses from PRRSv infection by knocking out the maternal CD163, Rowland states.
He further explains, in the simplest form, it begins with mating a wild-type boar with a knockout gilt or sow. “So, basically what you have done is create a protective shell around that fetus that has normal CD163,” Rowland says.
As a collaborative effort, MU scientists, using the CRISPR/Cas9 technology, executed it, KSU teams tested it and Rowland confirms it works. “We have eliminated reproductive PRRS. We have eliminated the disease with this technology,” Rowland says with excitement.
How practical is the research for real-world pig farming?
Rowland confirms it is a practical approach. The technology produces a healthy piglet protected from infection in the uterus. Since the pig still has the CD163 protein, it can be infected by PRRS during the growing stages. Nevertheless, other PRRS protection strategies such as vaccination and biosecurity measures can work in concert to protect the pig throughout its life.
“I always say PRRS is like a death by thousand cuts. It hits you in so many little ways in secondary infections, increases medications costs, increases mortality and lower health,” stresses Rowland. “If you can make sure that pig that goes into the nursery is PRRS-free and protected during the reproductive phase, it is such a positive thing.”
However, the technology to modify genes in animals is still subjective to regulatory approval. Researchers put the technology through its paces and gave it that farm-tough test. Still, it will be up to regulators and the consumer if the pork industry will be able to utilize it in the barns.
“One thing I do predict is this is going to be the future. The reason is the rationale is very straightforward. We are producing a healthy animal. That is the bottom line,” Rowland concludes.
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