Pigs with edited genes show resistance to costly virus
The process involves cutting out a small section of the pigs’ DNA, using a method known as CRISPR/Cas 9, according to the report in the journal PLOS Pathogens.
Tests of the pigs’ cells in lab dishes showed complete resistance to two major subtypes of Porcine Reproductive and Respiratory Syndrome (PRRS), a disease that can cause pneumonia in young pigs and fetal death in pregnant sows.
“Laboratory tests of cells from the pigs with the modified CD163 gene have confirmed that this change in the pig’s DNA blocks the virus from being able to cause infection,” said the report, led by the University of Edinburgh’s Roslin Institute.
The next step is to expose these actual pigs whose genes have been edited to the virus, to see if it makes them sick.
“Genome-editing offers opportunities to boost food security by reducing waste and losses from infectious diseases, as well as improving animal welfare by reducing the burden of disease,” said lead researcher professor Alan Archibald of The Roslin Institute.
“Our results take us closer to realizing these benefits and specifically address the most important infectious disease problem for the pig industry worldwide.”
The latest study is different from prior research removing CD163 – which also resulted in pigs not becoming ill — because only a small section of CD163 that interacts with the PRRS virus is deleted from the genome.
According to Ian Jones, professor of virology at the University of Reading, the approach is an “interesting” way to combat a virus for which there is no vaccine.
“The authors have removed part of the virus receptor, the cellular doorway the virus uses to initiate infection. If the virus can’t get in then disease is prevented,” said Jones, who was not involved in the study.
“The drawbacks of this approach are that all commercial stock would have to be bred to include this mutation, which takes time and public acceptance, and there is always the worry that the PRRSV virus would mutate to use a different receptor and so gain access by a ‘backdoor.'”
Further studies should “help address whether this is likely or not,” he added.