A UK-based research team has successfully harnessed gene editing technology to develop chickens with heightened resistance to bird flu, according to findings published in the prestigious scientific journal Nature Communications on October 11.

The team of researchers, led by Professor Mike McGrew from the University of Edinburgh’s Roslin Institute and Professor Wendy Barclay, Head of the Department of Infectious Disease at Imperial College London, employed cutting-edge gene editing techniques to enhance the chickens’ resistance to avian influenza.

Bird flu, a disease with a nearly 100 percent fatality rate in chickens, poses a severe threat to poultry populations worldwide.

The contagious virus primarily affects birds, including chickens, ducks, and wild birds, and has sporadically infected humans.

The avian flu virus, particularly the H5N1 strain, spreads through the air and respiratory routes.

The scientists focused on a specific gene, ANP32A, which the avian influenza virus relies on for replication inside the host. By editing the ANP32A gene in chicken embryos, they created birds with a genetically induced resistance to the virus.

The research involved exposing the genetically modified chickens to the H9N2 strain of avian influenza.

When challenged with a normal dose of the virus, nine out of ten gene-edited chickens remained uninfected, and the virus did not spread to other chickens.

Even when subjected to an artificially high virus dose, only half of the gene-edited birds became infected, and the transmission of the virus was minimal compared to non-edited chickens.

The genetic modification also limited the onward spread of the virus, as only one out of four non-edited chickens housed with the gene-edited birds became infected. The result underscores the effectiveness of the ANP32A gene edit in curtailing avian flu transmission.

Further analysis revealed that the virus adapted to utilize two related proteins, ANP32B and ANP32E, in the edited birds.

In cell culture experiments, it was found that some of the mutations may enable the virus to interact with the human version of ANP32, although replication remained low in human airway cell cultures.

By Ko Jae-won and Minu Kim

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