Breeding disease-resistant chickens through gene editing

650,000 people. Per year. The deaths were from respiratory illnesses related to seasonal influenza, according to the World Health Organization. It sucks, but (no matter how hard we try) there’s almost nothing we can do. We’ve been fighting it for almost 500 years, and now it’s winning the race again and again.The good news is we won’t give up

How to end the disease. We were able to find vaccines against coronaviruses in record time, and we have been able to eradicate at least two diseases: smallpox (1980) and rinderpest (2011). How can we continue to fail because of a disease that has been with us for over 8,000 years? I’m afraid the answer is simple: ending (or even controlling) a disease is not only a matter of money and technology, but also much more difficult than we thought.

In fact, our ability to eradicate disease depends more on the disease itself than on our efforts. First, the main characteristic of all “disappearance candidates” is that their natural reservoir is exclusively human (or, in the case of diseases such as rinderpest, the animal reservoir is a specific, easily identifiable species) ..

At least as our technology, health, and society evolve, “we can only aim to eradicate diseases that we can identify, monitor, and be able to intervene on a technically acceptable scale.” That means they must be difficult to cross the species barrier And diseases that are easy to track in open ecosystems.

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Influenza is not in that club. Influenza is a disease that spreads among birds, horses and pigs with surprising transmissibility. What’s more, the disease has the surprising ability to generate new subtypes in these animals and then return (full of innovations) to humans. That is, it is actually the opposite of an eradable disease.

But… what if there is another way? That’s the question they asked at the University of Edinburgh’s Roslin Institute, the animal research center where Dolly the sheep was bred. What if, instead of attacking viruses (or waiting for the flu to stop “hopping”), we turned to animals?

As? Change animals? indeed. You see, influenza A requires the protein ANP32A from chicken cells, which is key to its replication. What Roslin’s team did was use CRISPR to modify the gene behind the protein. This is both counterintuitive and wonderful: the resulting chickens are virtually free of the virus and certainly not contagious.

When the dose was a thousand times higher than normal, only half the people became infected.

When genetics closes a door, influenza opens a window. Because perhaps strangest of all, influenza quickly adapted to the lack of ANP32A and began using two other proteins (ANP32B and ANP32E) to replicate. They weren’t as effective, which is why it took so long for chickens to become infected, but it gives us a great example of how evil this disease can be.

However, the way is there. The proof-of-concept confirms that the technology’s applications are potentially limitless. Most importantly, because it allows the introduction of this type of mutation without compromising the animal’s ability to produce.

However, the most important thing now remains: ensuring that these genetic changes do not “cause” the virus to mutate, making it more dangerous.

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Photo | Travis Colbert

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