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Published on: November 5, 2012
Genetically modified pigs with CD163 point mutation are resistant to HP-PRRSV infection.
Ying Liu1, Lin Yang1, Hong-Yong Xiang1
1State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Animal Genome Editing Technology Innovation Center, College of Animal Sciences, Jilin University, Changchun, Jilin 130062, China.
Researchers identified a specific amino acid mutation (E529G) in pigs that confers resistance to Porcine Reproductive and Respiratory Syndrome Virus (PRRSV). This genetic modification significantly reduces viral loads without impacting growth or physiological functions, offering a promising strategy for PRRSV control.
Area of Science:
- Veterinary Virology
- Swine Genetics
- Disease Resistance
Background:
- Porcine Reproductive and Respiratory Syndrome (PRRS) is a major global swine disease causing significant economic losses.
- Current strategies for PRRSV resistance often involve large genetic modifications with potential growth performance concerns.
- Targeting specific functional amino acids offers a promising approach to develop PRRSV-resistant pigs with minimal physiological impact.
Purpose of the Study:
- To identify specific functional amino acids in CD163 that influence Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) proliferation.
- To evaluate the efficacy of a specific CD163 mutation (E529G) in conferring resistance to highly pathogenic PRRSV (HP-PRRSV) in pigs.
- To assess the impact of the E529G mutation on the growth performance and physiological functions of pigs.
Main Methods:
- Viral infection experiments were conducted on Marc145 and PK-15 CD163 cells to assess the effect of CD163 mutations on PRRSV proliferation.
- Pigs with the E529G mutation were challenged with HP-PRRSV, and viral loads were compared to wild-type (WT) pigs.
- Physiological indicators and CD163 scavenger function were examined in WT and E529G pigs.
Main Results:
- The mE535G and pE529G mutations in CD163 markedly inhibited HP-PRRSV proliferation by preventing viral binding and entry in cell lines.
- Pigs with the E529G mutation exhibited viral loads two orders of magnitude lower than WT pigs after HP-PRRSV challenge.
- No significant differences in physiological indicators or CD163 scavenger function were observed between WT and E529G pigs.
Conclusions:
- The E529G mutation in CD163 effectively confers resistance to HP-PRRSV in pigs.
- This genetic modification shows potential for breeding PRRSV-resistant pigs without adverse effects on growth or normal physiology.
- These findings provide novel insights for controlling future PRRSV outbreaks through targeted genetic strategies.
