Some phages developed small mutations in the proteins they use to attach to the bacterial surface – subtle changes that helped them avoid triggering Kiwa’s detection system. Others took a different approach: they allowed themselves to be detected, but escaped the consequences.
These phages carried mutations in a viral protein that seems to be involved in how Kiwa shuts down the infection. We don’t yet know exactly how this works, but the result is clear: with just a few changes, the virus keeps replicating, even after Kiwa has been activated.
This evolutionary flexibility is part of what makes phages so powerful, and why they hold such promise in treating infections. But it also highlights a key challenge: to make phage therapy effective, we need to understand how these microbial battles play out.
Rules of engagement
If a bacterial strain carries a defence like Kiwa, not all phages will succeed against it. Some might be blocked entirely. But others, with just the right mutations, might slip through. That means choosing or engineering the right phage for the job is not just a matter of trial and error – it is a matter of knowing the rules of engagement.
Studying bacterial defence systems like Kiwa gives us a deeper understanding of those rules. It helps explain why some phages fail, why others succeed, and how we might design better phage therapies in the future. In time, we may be able to predict which bacterial defences a given strain carries, and select phages that are naturally equipped – or artificially tuned – to overcome them.
That is the idea behind our growing . We are gathering phages from across the UK and beyond, including from public submissions – dirty water is often a goldmine – and testing them to see which ones can overcome the defences carried by dangerous bacteria. With over 600 types already catalogued, we are building a resource that could help guide future phage therapy, pairing the right phage with the right infection.
Kiwa is just one piece of the puzzle. Bacteria encode many such defence systems, each adding a layer of complexity – and opportunity – to this microbial arms race. Some detect viral DNA directly, others sense damage or stress, and some even coordinate responses with neighbouring cells. The more we learn, the more precisely we can intervene.
This is not a new war. Bacteria and phages have been locked in it for billions of years. But for the first time, we are starting to listen in. And if we learn how to navigate the strategies they have evolved, we might find new ways to treat the infections our antibiotics can no longer handle.