Gene-edited Pigs are Resistant to Billion-dollar Virus
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Scientists have produced pigs that can resist one of the world’s most costly animal diseases, by changing their genetic code. Tests with the virus – called Porcine Reproductive and Respiratory Syndrome, or PRRS – found the pigs do not become infected at all. The animals show no signs that the change in their DNA has had any other impact on their health or wellbeing.
PRRS costs the pig industry around $2.5 billion (£1.75bn) each year in lost revenue in the US and Europe alone. The disease causes breathing problems and deaths in young animals and if pregnant sows become infected, it can cause them to lose their litter. The virus infects pigs using a receptor on their cells’ surface called CD163. Researchers at the University of Edinburgh’s Roslin Institute used gene editing techniques to remove a small section of the CD163 gene. They focused on the section of the receptor that the virus attaches to, leaving the rest of the molecule intact. The team collaborated with Genus PLC, a leading global animal genetics company, to produce pigs with the specific DNA change.
Previous studies had shown that cells from these animals were resistant to the virus in lab tests. This is the first time researchers have exposed these pigs to the virus to see if they become infected. They found that none of the animals became ill when exposed to the virus. Blood tests found no trace of the infection. "These results are very exciting and further underscore the potential, through gene editing, to provide incredible benefits to the global pork industry, and society as a whole, by improving animal health. We look forward to further collaboration with the University on this exciting project." said Jonathan Lightner, Chief Scientific Officer, Genus PLC.
PRRS is endemic in most pig producing countries worldwide. Vaccines have mostly failed to stop the spread of the virus – which continues to evolve rapidly. Other groups have used gene editing to create PRRS-resistant pigs by removing the whole CD163 receptor.
Removing only a section of CD163 allows the receptor to retain its ordinary function in the body and reduces the risk of side effects, the researchers say. Lead researcher, Dr Christine Tait-Burkard, said longer-term studies would be needed in order to confirm the genetic changes do not have any unforeseen effects on the animals. Dr Christine Tait-Burkard, Career Track Fellow at The Roslin Institute said, "If these studies are successful and the public are accepting of this technology, we would then be looking to work with pig breeding companies to integrate these gene edits into commercial breeding stocks."
Genetically modified animals are banned from the food chain in Europe. It is not clear what regulations would apply to gene-edited animals, however, as the approach is different.
GM techniques have been controversial because they can involve introducing genes of other species into an animal. In contrast, gene editing speeds up processes that could occur naturally through breeding over many generations, without introducing genes from other species. The teams says the research should prompt public discussion on the acceptability of gene-edited meat entering the food chain, to help inform regulation of the technology. Jef Grainger, Associate Director, BBSRC Science Strategy, said, "This is an exciting result that demonstrates the potential for genome editing approaches to enable significant improvements to be made in the health and welfare of farmed animals, and reduce the economic impacts of diseases that are otherwise difficult to manage effectively."
This article has been republished from materials provided by the University of Edinburgh. Note: material may have been edited for length and content. For further information, please contact the cited source.
Reference: Burkard, C., Opriessnig, T., Mileham, A. J., Stadejek, T., Ait-Ali, T., Lillico, S. G., … Archibald, A. L. (2018). Pigs lacking the scavenger receptor cysteine-rich domain 5 of CD163 are resistant to PRRSV-1 infection. Journal of Virology, JVI.00415-18. https://doi.org/10.1128/JVI.00415-18