‘What we want to do is basically stop people dying’

It was during his A-levels that Barney found an interest for infectious diseases.

‘I was at Elizabeth College in the 2000s and I remember I really liked the biochemistry part of biology – which I don’t think anyone else really enjoyed that much,' he said.

'I think because you cover so much content in your GCSE and A-levels, they obviously can’t go into too much detail, so they would say things like, “Oh, this cell signals to another cell, or this cell tells this cell how to do something,” and for me, I really wanted to know how a cell does actually talk to another cell, how does that actually work?'

‘I think it was looking at diseases in A-level biology – infectious diseases in particular – that I wished we could do more of it. Unfortunately, we then had to move on to ecology, which I did not enjoy – lots of standing on the shore counting seaweed, which now sounds like a great afternoon – but as a 17-year-old, that wasn’t that exciting.

‘I was really fascinated about different diseases, how they invade the body, what they do to you and how you can stop them.’

Barney’s interest in diseases grew during a year in America as part of his biochemistry degree at the University of Bath.

‘I worked at the University of Georgia infectious disease unit in their veterinary college and I worked on worm parasites – nematodes – and I think that’s really where I got into tropical diseases and parasites in particular, because I just found them really fascinating,’ he said.

‘From there I did a masters in microbiology at Bath and I then went to Oxford actually to work. I worked for a biotech company for two years doing gene therapy and then after that started my PhD at the University of Oxford working on malaria vaccines, and I’ve been there for nine years.

‘It was a bit of a last-minute decision to go to America. The opportunity arose and I remember I was sitting with a friend and we were both, “I’ll go if you go” – we both weren’t sure. We both went to different labs and I think I picked it because the project was on these parasites and it had a real-world application.’

After developing the vaccine – which is now in clinical trials – for his PhD, Barney has been working out how that vaccine works and will now focus on redesigning it to make an improved version.

‘Malaria has been around forever. There was about 280 million cases in 2024 and there’s about 600,000 deaths each year, so what we want to do is basically stop people dying and stop people getting infected with malaria,’ he said.

‘Malaria has a reasonably complicated life cycle. One part of that life cycle is where the malaria parasite invades red blood cells, it will then replicate in the red blood cell, and then 10 will burst out and then they’ll invade 10 new red blood cells, so you get the cyclical infection of red blood cells and that’s what causes all the disease symptoms.

‘What we want to do is make a vaccine that blocks the malaria parasite from getting into that red blood cell. The way we describe it is that the malaria parasite has lots of keys that they can use to unlock the red blood cell and get in, so normally what we want to do is block that lock, to have a vaccine that basically makes antibodies.

'Those antibodies block the lock and then the key can’t go in, that’s how it would work. However, we have this protein that we’ve developed into a vaccine and basically we didn’t know why it blocked invasion – this protein isn’t one of those keys.

'We knew that the vaccine could block invasion, but we didn’t know how. What we did – because we want to improve the vaccine and you can’t improve the vaccine unless you actually know how it works – is we got this panel of antibodies, which are proteins that are made by the immune system. We had over 80 of them and what you’re hoping for in this situation is that you find some of the antibodies don’t do anything, some of them block, and some of them are really effective at blocking. Then you would look at how those really effective ones stop invasion, and that’s what you would build your vaccine around.

‘Of the 83 antibodies, none of them did anything at all. We know the vaccine works, but none of our antibodies did anything on their own, so that was the puzzle that this piece of work is. What we found is that when you start mixing them in combinations, then you start blocking the malaria invasion and then you start stopping that parasite from going in. What we found is that the protein that they target is this bridge protein – it bridges the parasite and the red blood cell and it’s really flexible. What we found is that if these antibodies stick onto the bridge protein, then rather than being flexible it stiffens and it can’t move, it can’t do its job and that’s how this vaccine is essentially working.’

It took five years after his PhD for Barney to work out how the vaccine worked.

‘It’s more of a relief, to be honest, there was a lot of years and meetings where me and my colleagues would just be staring at data, going “We don’t know what this means”’, he said.

‘This is quite different from a school or a university project where you know that there is an answer that you’re meant to get to and someone can help you find it. Here we just have a bunch of antibodies, we do some experiments, and we don’t really understand the results. So then we just have to think, “Okay, what’s the next sensible experiment to do?” and you just keep chipping away at it until eventually it comes together into this picture. I think it was more relief that after five years we had actually got something that made sense and that we could actually use to progress, rather than five years kind of down the drain.’