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CRISPR-edited chickens showed strong but incomplete resistance to one avian flu strain in a controlled study. After a low-dose exposure to H9N2-UDL, nine of ten edited birds remained uninfected; at 1,000 times that dose, infections broke through. The result is a proof of concept, not evidence that chickens cannot catch bird flu.

What did researchers change in the chickens?

In a 2023 study, researchers used CRISPR/Cas9 to alter the chicken ANP32A gene, introducing two amino-acid substitutions: N129I and D130N. The edits were intended to disrupt an interaction between ANP32A, a host-cell protein, and influenza virus polymerase, which the virus relies on to reproduce.

The work focused on H9N2-UDL, a low-pathogenic avian influenza strain. It did not test every bird-flu strain or establish how the edited birds would respond to infection in farms or other field conditions. The study, published in Nature Communications on 10 October 2023, used two-week-old birds for its direct challenges.

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Could the edited chickens still catch bird flu?

Yes. The outcome depended on the exposure dose. In the low-dose challenge, researchers inoculated each bird with 103 PFU of H9N2-UDL. Nine of the ten edited chickens remained uninfected. The one reported infection was low and transient, and researchers observed no onward transmission in that experiment. The Roslin Institute also reported that the virus did not spread to other chickens in the trial.

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When the inoculum was raised to 106 PFU per bird—1,000 times the low-dose amount—breakthrough infections occurred. Viruses isolated from edited birds had polymerase mutations associated with adapting to the edited ANP32A protein. In other words, the edit made infection harder under the lower-dose conditions tested, but did not make infection impossible.

Why might one gene edit not be enough?

Chickens have other ANP32-family proteins, including ANP32B and ANP32E. The study found that breakthrough virus could use these proteins. Removing ANP32A alone did not eliminate all viral growth in the reported chicken-cell experiments; editing ANP32A, ANP32B, and ANP32E together did eliminate viral growth in those experiments.

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That cell result is not the same as proving that a three-gene edit would safely protect live chickens. The authors cautioned that extensive editing could harm animal health or fitness. They described the work as a first proof-of-concept step and said multiple genetic modifications would be needed to curtail viral escape.

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What did the study find about health and egg production?

In a preliminary assessment, the researchers reported no observed differences in growth, external appearance, behaviour, or vaccination response between edited and unedited birds on the measures they examined. The small assessment does not establish long-term health or commercial-scale performance.

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For egg production, four edited hens began laying at 20 weeks of age. Over a two-month observation period, they produced an average of 5.75 eggs per hen per week, which the study described as comparable to wild-type hens. Four birds and two months of observation are not enough to establish long-term or commercial productivity.

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What the result does—and does not—show

  • Shown: An ANP32A edit was associated with substantial resistance to H9N2-UDL infection in a low-dose, controlled challenge: nine of ten edited birds remained uninfected.
  • Also shown: Higher-dose exposure led to breakthrough infections and viral changes associated with adaptation.
  • Not established: Protection against all avian influenza strains, performance in field conditions, long-term safety, or commercial-scale productivity.
  • Not established: Commercial availability or regulatory approval of these gene-edited chickens. The animals were bred and maintained under UK Home Office licensing, and the challenge work took place in regulated research settings.
  • Not addressed: Protection for humans. This chicken study does not demonstrate that gene editing prevents human influenza or removes public-health risks from bird flu.

For the evidence and experimental details, see the original Nature Communications paper and the Roslin Institute’s summary.

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