GE-CD163 pigs were generated using CRISPR/Cas9 gene editing in pig zygotes.

Porcine reproductive and respiratory syndrome virus (PRRSV; new name: Betaarterivirus suid 1) is causing late-term abortions, stillbirths, and respiratory disease in pigs, leading to major economic losses to the worldwide pig industry. GE-CD163 pigs inoculated with PRRSV-1 (strain BOR-57) were resistant to viral infection.

In GE-CD163 pigs, exon 7 of the cd163 gene has been excised using two guide RNAs targeting the intron up- and downstream of exon 7. The gene edit results in a deletion of 105 amino acids and a single amino acid substitution in the CD163 protein, leading to the loss of the PRRS virus interaction site, the scavenger receptor cysteine-rich domain 5 (SRCR5). cd163 expression and biological function of its protein remained unchanged.

Heterozygous pigs were bred to yield homozygous GE-CD163 animals. The edited CD163 gene was found to segregate according to Mendelian rules of inheritance for a single genetic locus.

Sources:

1. Burkard et al. (2018), Pigs Lacking the Scavenger Receptor Cysteine-Rich Domain 5 of CD163 are Resistant to Porcine Reproductive and Respiratory Syndrome Virus 1 Infection. Journal of Virology 92:e00415-18.
2. Burkard et al. (2017), Precision engineering for PRRSV resistance in pigs: Macrophages from genome edited pigs lacking CD163 SRCR5 domain are fully resistant to both PRRSV genotypes while maintaining biological function. PLOS Pathogens 13:e1006206.
3. Health Canada: Decision Document DD2026-159: Determination of the Safety of PIC-Canada Ltd.'s Pigs (Sus scrofa) Resistant to Porcine Reproductive and Respiratory Syndrome Virus (as of January 23, 2026)