It was snowy and Tottenham Court Road was frozen over when I had my interview at the Middlesex Hospital. I’d got smart shoes on and fell over three times. But I passed the interview and started my training on 8 March 1982.

Little did I know how busy and all-consuming things were about to be.

The 3-year training was ward-based and, after six weeks, it was straight into the hospital as part of the workforce. It was there encountered my first HIV case: an American, with terrible lymphatic swelling of his legs, the disease advanced. There were no barrier measures. In 1982, news of HIV was just breaking, creating a sense of unease within the department. Reports were coming from America but very little information of any use. There was consensus that it was transmitted through sexual activity, and mainly affected gay men, alongside a horrible prevailing sense that it was their problem. We didn’t have an HIV ward at that time.

In the earliest days, we saw men in their 40s or older. They’d been travelling, had bigger groups of friends. They were more likely to become infected than someone young.

Over the next year, further patients began arriving quite regularly, usually in advanced states of illness. In a side ward, I met Colin, another American. Suddenly we had barrier nursing – gloves, masks, aprons. It seemed very over-the-top. But people were allowed to come in and visit him without it. I didn’t understand. And I didn’t like it. I’d be all dressed up for a night out and I’d visit him before I went. No one stopped me. I felt an acute sense of injustice: either everyone should wear it, or no one.

It was quite clear that, whatever this was, it was taking significant numbers of people out. By the time I completed my training, I knew I wanted to be involved. This wasn’t something that you could just stand by and watch. I didn’t feel scared because I didn’t believe it was transmitted through everyday contact. I applied to do a course in sexually transmitted disease (which didn’t include HIV then), and that’s when my involvement began in earnest.

I applied for a research nurse post at James Pringle House, where I was put on the first clinical trial team: the Medical Research Council Concorde trial. It was AZT, azido thymidine, versus a placebo, in asymptomatic patients, of whom we recruited 87. We had no viral load measurements; that was still a long way off. We did have CD4 – immune counts – but we didn’t really know what they meant. There was suspicion about the drugs, though some people had seen serious illness among friends and people abroad and were desperate to get involved.

I saw patients every two weeks at the beginning. I took bloods and checked results, making sure they’d got their medications. It was a placebo-controlled, double-blind trial, so I didn’t know who was taking active medication. But I noticed, on reports coming back from the haematology department, one of the values increasing over the first 8-10 weeks. I phoned to ask, ‘Why is this level going up in some of my patients? What does it mean?’ Actually, one of the effects of AZT is that cellular volume goes up, which effectively ‘unblinded’ the trial. It was panic stations with MRC. All laboratories had to block those results. I was pleased I’d noticed. I wonder, though, how others missed it.

Most people remained well for the first six months of the trial. Thereafter we began to see that, whatever the medication was doing, it probably wasn’t  going to be enough. Little did we know how long it would take before there were really effective medications and, at that point, we didn’t know how important continuing to take medication was. People would be on and off it. AZT has a side effect in some people that makes them quite nauseated in the first 2-4 weeks. If people carried on they get over that, but we didn’t know that then. So we were making people who already didn’t feel great, even worse.

On top of the trial drugs, patients had opportunistic infections that were also medicated. Some patients had an awful lot of drugs to take. In the early days, it was industrial quantities of antivirals, antifungals, antibiotics. There was the awful cat and mouse nature of keeping terrible infections like Cryptosporidium diarrhoea at bay. Today, if people say they’ve got ‘diarrhoea’, it means they’ve been twice before they left the house, not that they’re losing 16 litres of liquid a day. It was horrifically debilitating. Some would be enormously unwell, not just a rash and sweats, but meningitis. A reaction like that would require hospital admission. I hated feeling that when people did become really unwell, and were admitted to a ward, I could do nothing more. At that point, I felt very deskilled. It was a goodbye in most cases.

The deaths really started to go up from 1983-1984. Not just in my patient population, but in the HIV-positive individuals being seen at our department. A positive diagnosis meant death. So many deaths. You didn’t have time to pick yourself up before you found out someone else was positive.

I was seeing more of these men – there were only one or two women – than I was seeing of my friends or family. I didn’t talk to many people. What was there to say? My work was confidential, and often harrowing. It doesn’t make good conversation at a pub or restaurant. People would say, ‘Aren’t you scared?’ And I’d reply, ‘No, I’m not having sex with my patients. Why should I be?’

But I’d watch friends, lovely men, melting in front of me. You could see someone from behind, the square of their shoulders, the shape of their neck. You could tell, and you’d think, oh god. There was a lot more of it around than people were actually talking about.

Quite quickly, 2-3 years into the Concorde trial, was Delta, with two medications rather than one – double therapies. DDC, deoxycytidine, could cause people nasty mouth ulcers, but was more tolerable in terms of general physical effects. DDI – didanosine, had to be mixed with water and made an unpleasant drink. One element would be a placebo. It wasn’t very effective and there was a bigger mistrust in the drugs by then.

Then came the government advert in 1986. AIDS: Don’t Die of Ignorance. It was designed to scare. And it did. But it went too far, demonising people with HIV, and the whole situation. It gave people permission to blame men that had sex with men.

At some point within that first couple of years, we realised that people with lower CD4 counts needed protection, prophylaxis, for pneumocystis careniae pneumonia [PCP], one of the biggest causes of death in HIV infection if left untreated. That probably made a bigger difference. We were learning more about HIV, even though the medication wasn’t doing what was hoped.

But we didn’t know that people might stop taking their medication for a few days if they didn’t feel well, then restart it. We didn’t know about viral resistance and how constant pressure on viral replication was important. It wasn’t until much later on, when we first had viral load tests, that we realised how quickly viral load could rebound if medication was stopped, and also found out more out about managing people to take the drugs therapy: it’s got to be practical, they’ve got to be tolerable. If you make something impossible for someone, why should you expect there to be good results? You’ve got to find something that may not be the optimum that scientists and virologists want, but that is attainable. They wanted people to be setting alarm clocks to get up at five and take something on an empty stomach. Then take something else with a high-fat meal two hours later. Instructions to crush pills, mix with brown apple juice, not cloudy, otherwise there would be an interaction. It was too complex.

There were drug interactions. One trial patient died because he was taking an over-the-counter antifungal medication. He should’ve told us. He ended up getting pseudo membranous colitis, and he died. I felt absolutely dreadful. The doctor in charge of the study tried to tell me there was nothing I could’ve done. But if it wasn’t for the trial, he wouldn’t have died. And you take that away with you. It’s still with me more than 30 years later.

People had very personal reactions which caused them to stop taking therapy. I remember one chap coming in after Freddie Mercury died, saying he’d stopped his therapy because he felt that Freddie Mercury’s death was probably to do with his treatment. It was difficult because there wasn’t detailed information to contradict him. There was also anger about side effects from drugs by this point. And impatience from both patients and the medical profession. Everyone was working so hard but losing so many people. You just thought, when’s it going to stop?

A glimmer of hope came by 1993. I remember one of the studies showed some people picking up. We weren’t sure, until the end of the study, when they were unblinded. But you could see that viral loads were dropping down and equated to people feeling clinically better. It was a much-needed glimpse of a brighter future, because by that point it was getting very tough.

I drank most evenings when I got in. It was accepted as a coping mechanism. You didn’t really have enough time to think about it. Get in. Drink a bottle of wine. Preferably walk the dog first. Get up the next morning. Walk the dog. Off to work. And repeat. As nurses we didn’t have supervisional support. I’d meet up with other nurses from the Royal Free and the Chelsea and Westminster, maybe only once or twice a year, at clinical trial meetings to discuss the progress of the trial. Occasionally, if there’d been something traumatic, a drug interaction, perhaps, you’d be able to talk to your peers. Otherwise you were on your own. You didn’t talk about it. They were very difficult times. I started to think, can I keep doing this? Can I really keep doing this?

But when triple therapies come along, you could see that people who were underweight, or had skin manifestations, were actually improving clinically. Their energy levels were better, they had fewer opportunistic infections, or less serious ones like oral candida. And by this point, we had viral load measurements. You could also see those who weren’t able to keep taking the drugs deteriorate by contrast. I felt frustrated. You can’t drive people to stick to something that, for whatever reason, they don’t feel able to. You can only try and encourage.

That first study wasn’t powered to show that the three medications together were better. I could see it. But that’s all I could do. It was anecdotal. Still, some of them made it! Even though they were really on the brink on the brink of death, by the grace of God, they made it. And some of them didn’t. I’m absolutely sure that some people JUST missed the boat.

In the end we found effective therapies. We did a research paper on Kaposi’s sarcoma virus. People with detectable levels in their bloodstream went on therapy and we saw, not only that their HIV viral loads fell, but their KSHV viral loads fell too. We knew that it was real and progressive improvement. We were finally seeing the turnaround, the benefit from therapies. That’s why I stuck with it. Otherwise, I’ve no doubt that by 1995 or 1996, I would’ve left. By 1997, things were doing well with the treatment advice clinic.

It was a long journey, but I’d been there from the beginning.

I returned to the NHS at the start of the Covid pandemic, joining the vaccination programme. In some ways, the beginning of Covid felt similar: the fright, the suspicion, the insistence that we must find out where it came from! I thought, no. Let’s find out how to deal with it, and worry about that later. I continued to work in HIV, specialising in HIV treatment advice and support until 2017 when I left my post and London. To the end, I was still seeing some of the patients that I had met during the first clinical trial in the 80’s. We had made it through together! My career and most importantly my patients have been the greatest part of my life, and I will carry that with me forever.