It's a real privilege to be able to tell you about a pandemic and not the pandemic that we have all recently experienced, but a pandemic which was first recorded in the early 1980s, the AIDS pandemic. In the early 1980s, being diagnosed with AIDS was a death sentence. Life expectancy was around 12 months after diagnosis. But through some extraordinary science, now, 40 years later, people diagnosed with the virus that causes AIDS have a normal life expectancy. They have undetectable virus levels within their body and they can't transmit the virus. So today I want to tell you about these advances, how these medicines work, and how how this extraordinary transformation was brought about. But still, 41 million people have HIV today, and it was 1.2 million new infections in 2025. So I also want to tell you some of the challenges that we face because of this continuing AIDS pandemic and what modern science is trying to do to prevent it. So first I want to take you back to the early 1980s. Princess Diana was getting married to Prince Charles. The other side of the Atlantic, the first space shuttle was uh was zapping off into orbit. Um, Dynasty was on the television with big haircuts and huge shoulder pads. Um and um the first reports of a serious illness started to come in. And this was the very first medical report of a new disease. Five young gay men were diagnosed in Los Angeles with a fungal pneumonia. Um and uh fungal pneumonias are serious illnesses, uh they start with um uh a lack of ability to breathe, um, a cough, but they can really develop into a life-threatening condition. And young, healthy people uh don't normally get pneumonia of the lungs like this. It was very noteworthy. Um a few months later, a dermatologist in New York uh reported this particular type of skin cancer. Um, a cluster of these skin cancers caused kaposi sarcoma, um, again, in young, healthy, uh, or previously healthy gay men. And again, this is very unusual in healthy people uh with a normal healthy immune system. But the New York Times reported a month later that 41 cases of this cancer had developed, and 24 and uh eight of the victims had tragically died. So, what linked these two clusters of unusual um illness? Um, in both cases, the infectious diseases, um, and in both cases um the the people suffering from these diseases showed very low levels of a particular part of your immune system called the C D4 plus T cells. And these are a crucial component of immunity, uh, which is important for tackling and responding to infectious disease. In other words, uh, these people seem to have impaired immune systems, and their impaired immune systems were causing them to be susceptible to diseases or infections to which they would not normally be susceptible. How did this develop? We can sort of see the development uh of this uh disease through the things that it was called in the press. It started in the early 1980s uh to be called GRID in one article in the New York Times, gay-related immune disease. But quickly, it was found in other groups of people. It was found in people injecting uh drugs such as heroin. It was found in hemophiliacs using blood products uh to help manage their hemophilia, and it was found in Haitian immigrants in New York. Some Bright Spark decided to call it the 4 H's disease. Um, but it was really rapidly within within very few months, um, people started to realize that anybody, of course, uh could uh be afflicted by this particular illness. Um, it was found in all groups independent of their sexuality, their nationality, or their previous health conditions. And so it was called AIDS or the acquired immunodeficiency syndrome. So, what was it like to have AIDS in the 1980s? I'm going to show you a challenging picture. Um, this on the left is uh David Kirkby, um, towards the end of his life from AIDS. And he and his family allowed this picture to be uh in in Life magazine to illustrate that AIDS was a really horrific way uh to die. Um, the immune system of the patient uh loses function, and as a result, they become susceptible to all sorts of different infectious diseases. Um, we've already met two of them, but fungal infections of the mouth of the airways make it hard to eat or to swallow or to talk. Um, cancers caused by viruses can develop, and gradually, as their immune systems try to fight all of these simultaneous infections, um, they waste away. And as I mentioned at the beginning, to begin with, AIDS detection being diagnosed with AIDS was a death sentence. Uh, you had a month, a year left to live. But the physical symptoms weren't all of the problem because um because uh the the those early sufferers from AIDS um uh and and the way in which the press represented them, um, stigma was also a problem uh for early AIDS sufferers. And this is a quote uh from Lorna, um a senior nurse in Edinburgh in an HIV clinic. Laura wrote, We realized how different it was from other diseases, how badly the stigma isolated people, isolated them to the point that I am the only person they have talked about their deep feelings to, as they have no one else to share that with. And that really broke my heart. So the 1980s um saw this this uh yeah, this this terrible disease. What did our governments do about it? So public health messaging uh started to kick in around 1985. It was the Reagan administration in the United States, and it was the Thatcher government in in the United Kingdom. Um, and uh those governments didn't tackle the AIDS, the AIDS uh problem or uh or illness uh for a long time. Um but but by 1985, 1986, they'd really started to share the message of AIDS. So this is Norman Fowler, uh the health minister in the mid-80s, and he launched this big campaign, the AIDS Don't Die of Ignorance campaign. They delivered uh some um 30, 23 million uh leaflets were delivered to 23 million households, and a public health campaign uh was put onto the television, again with incredibly stark adverts. I'm going to show you one of them. So, this advert uh was aired on the BBC in the mid-80s.

There is now a danger that has become a threat to us all. It is a deadly disease, and there is no known cure. The virus can be passed during sexual intercourse with an infected person. Anyone can get it, man or woman. So far, it's been confined to small groups, but it's spreading. So protect yourself and read this leaflet when it arrives. If you ignore AIDS, it could be the death of you. So don't die of ignorance.

Pretty stark stuff. Those of you around in 1986 will probably remember it. 11-year-old me certainly remembers it, and uh it convinced me that sex was a very bad idea for a while. Um, so um, so this pandemic uh was was really challenging for huge reasons. Um, but subsequent public health campaigns uh started to kick in um to help people to understand some of the misinformation that came from those early public health campaigns or or the preconceptions that came. Firstly, that AIDS can affect anyone, secondly, the ways in which people can't um be affected by AIDS, or ways that you can't catch AIDS. You can't catch it from a public pool or from a glass, for example. It's safe to shake hands with an AIDS patient, it's safe to spend time uh with them. So, this was where AIDS was by the mid-1980s. Uh, the challenges of AIDS and the shock of AIDS, uh, this really uh challenging disease. So now I'm going to tell you um an optimistic story and a really positive story. Um, know your foe. Uh what causes AIDS and how can we stop it? So, how does scientific progress take us from those times to a time when AIDS could be prevented, or at least uh the the symptoms of AIDS uh treated and prevented? Know your foe. So the cause of AIDS was first discovered in the Pasteur Institute uh in Paris in 1983 by these two researchers here, Professors Montagnier and Bar Sinuset. Um and they were experts in a group of viruses called the retroviruses. These extraordinary uh viruses um had previously been shown to be able to infect um CD4 T cells, just like the viruses that cause AIDS. And a group of French physicians went to see these two researchers to say, let's find out if if retroviruses or if AIDS may be caused by a retrovirus. Um and and uh Barcinesset and uh Montagnier had uh an assay that they could use to tell whether there was a retrovirus in a sample. It comes, uh this this um this assay uh looks for a particular molecule called a reverse transcriptase, which we'll meet in subsequent slides. Um they took a sample uh from a French um uh man who was um seemed to be in the early stages of having AIDS, they took a sample of one of his lymph nodes and they put it into their assay. Um, and uh they found uh indeed that there was reverse transcriptase present. This sample contained a retrovirus. The gentleman on the on the right there, Robert Gallo, was an American researcher, and he was performing similar experiments uh in Washington at around the same time. And again, he took samples from a number of AIDS patients and found the same retrovirus in them all. And this was that retrovirus, the human immunodeficiency virus. So, as in any case we want to tackle a new disease, uh the challenge was to understand this disease and to find out what its Achilles' heels are, what are the parts of this vir uh disease, this virus that one can tackle? So this is a schematic. Well, on the left here is the virus itself, um, the virus HIV that causes AIDS, and on the right is a schematic of one of those virus particles. So we see this uh circular uh virus uh made up of multiple layers. So right in that central layer is the blueprint which directs the production of virus particles. In this case, it's a blueprint made of the molecule RNA that is surrounded by a capsid, that sort of bullet-shaped green structure on the right-hand image, made of many copies of the same protein. And this is a delivery device for that blueprint. And then outside that is an envelope, the circle you can see there, which is a membrane, much like the membranes that wrap around our cells. And the blue spikes are a viral protein which is used by the virus to detect our cells. So this is the HIV virus. So, how is it different from the cells of our body, and how can we use that information to work out how to stop it? On the left there represents one of the cells of our body. They also contain a blueprint made of the molecule DNA, very much like the molecule RNA, which makes the blueprint at the core of the virus, um, but in in in but also different. They're both uh strings of coding information made in molecular form, um, and they're highly related to each other, uh, but not identical. So the DNA molecule within our cells is held within this structure called the nucleus, um, and then the DNA directs the production of RNA, um, and then that tells our body how to make protein molecules, which form all of the machinery which builds and uh creates um our cells. So, how how is the virus different? Well, I've already mentioned that rather than containing a blueprint coded from this molecule DNA, the virus contained a blueprint coded from RNA. And it did this really unusual thing which um which our cells uh don't do. It can take, you'll see, you'll see now there's an arrow going from RNA backwards to DNA. Because the RNA blueprints that make up the core of this virus could be converted into DNA. That's not something that our cells do. And the reason why this virus does this is because by creating a DNA copy, that DNA can get inserted into the DNA of one of our cells, and it can hide away in those cells through a process called latency. And the reverse transcriptase, this famous enzyme that all of these retroviruses have, that allowed the virus HIV to be discovered in the first place, that's the enzyme which creates this DNA copy. So this shows you the life cycle of the virus. So the pink bit on the lower part of that diagram is the cell, the cell, um in this case, one of our cells within our body, these immune cells, these CD4T cells that I described earlier. And up at the top left, you can see the virus particle. You can see it docks onto our cells using those spikes that emerge from the virus, those envelope proteins, and it docks onto receptors on the cell surface called CD4 and CD44, uh CCR5. And that allows the viral membrane to fuse with the cell membrane, delivering that bullet-shaped capsid into our cell. That works its way down, following down the left-hand side, until it's inserted itself into the nucleus, where it releases the where it copies its RNA blueprint into DNA and releases that viral DNA you can see at the bottom. Next, a molecule called integrase, also from the virus, takes that viral RNA, DNA copy and integrates it into the DNA of our own cell. The period between getting infected with HIV and developing the symptoms of AIDS can be 10 to 15 years. And this integration process explains why. Because the virus DNA gets inserted into the DNA of our cells and it hides there within our cells, undetectable. But when the trigger comes, our cells start to make RNA copies of that DNA. They leave the nucleus into the main body of the cell, they produce viral proteins, and on the top right, you can see those viral particles budding off. So this life cycle helps researchers to understand why this virus damages the immune system. It's the specific recognition of this CD4 receptor, which means that this virus specifically targets these classes of immune cells, the CD4 plus T cells. And this is an incredible strategy for a pathogen because these are exactly the same cells which would fight the pathogen. So by infecting and destroying those cells, the pathogen is destroying the components of our immune system, which would otherwise be the part of the first line of defense. And I've already mentioned this integration of the DNA causing latency, allowing the virus to hide away inside our cells. But the life cycle also showed opportunities for the virus. The reverse transcriptase, the integrase, these are things that our cells don't have, things that our cells don't do. So they provide a great opportunity to develop a medicine which targets something specifically in the virus, which won't affect molecules from our own body and cause side effects. The protease that you see labeled up there on the top right is really important for the maturation of the virus particle. And again, that's not something that our bodies or our cells do. So knowing their foe, researchers were next able to develop medicines which target some of these different components. And we'll see medicines hitting each of the integrase, the reverse transcriptase and the protease. So these antiretroviral therapies, which now mean that those who have access to these medicines can live normal life expectancies with an HIV infection. What do these medicines do and how do they work? And when did they come about? The first of these medicines was called AZT. Um and it was uh licensed for use in humans in 1987. Um it wasn't originally developed as an AIDS medicine, it was originally developed as a cancer medicine. Um, but researchers at uh Wellcome Borough, Borough Welcome Company in the United States, um, thought that it might stop the function of the reverse transcriptase. So, how does it work? So AZT is there on the left, and thymodine is there on the right. And thymidine is one of the building blocks that the blue the that DNA molecule that forms the blueprint of our cells is is made from. It's made of many copies of four molecules like thymodine joined together. And to join them together, um, if you look at the bottom, there's an OH uh chemical group. And then on the left hand side, there's an OH chemical group as well in thymidine. The OH from one of those molecules joins onto the OH of another thymodine or related molecule, making a chain, creating the codes, the blueprint. But you'll notice that AZT in the place of that OH molecule has those three Ns. Um and that chemical group uh can't link on to another building block. It's called a chain terminator. So the reverse transcriptase, if it incorporates that AZT molecule into the growing DNA code, that DNA code can't grow any further, it gets prevented from growing. So, in other words, this AZT molecule could stop the reverse transcriptase from working and it could stop the development of the DNA copy of the RNA virus. And without the ability to make that DNA, the virus is not able to replicate anymore. So AZT was the first medicine that was used. In fact, until 1993, it was the only licensed medicine that could help AIDS patients. Um was it effective? Um it was a lot better than um not having AZT. Um it was uh estimated in studies to maybe lead to three-to-fold, fourfold um increased life uh expectancy for somebody diagnosed with AIDS. But it also had substantial side effects and resistance to AZT would develop often within around one year within a patient. Um and if that happened, um, that would limit its effectiveness or prevent its effectiveness. Because this virus is very fast at mutating and changing. So AZT was the first AIDS medicine, but it wasn't the medicine which led to normal. Life expectancy for AIDS patients. So instead I mentioned the maturation of the virus particle. You can see on the top right there these HIV particles budding off from a CD4 T cell, creating on the bottom left these, sorry, on the left side, on the bottom left, this immature virion. So this is a budded virus particle, but it hasn't matured. You can see that that bullet-shaped structure in the core of that virus hasn't yet developed. So that immature virus is not infective. It can't infect somebody's, another cell, and it can't replicate anymore. And what needs to happen is this maturation process where this molecule called the protease snips some of these proteins in the immature virion, allowing them to form this capsid and allowing a mature virion to form. On the left hand side there, you can see what this protease molecule that does that maturation looks like. And on the right, you can see right at the core of that protease molecule, you can see the peptide that it's cleaving and cutting. And researchers were able to develop molecules like sequinavir, which was developed by Roche, which can block up this protease and stop it from functioning, preventing uh viral maturation. Sequinavir was licensed sometime in the around 1997. And these HIV proteases inhibitors, as they were called, had an extraordinary effect. Firstly, researchers realized that they shouldn't be given alone, because giving a medicine alone makes it easier to develop resistance to that medicine. But if you combined these HIV protease inhibitors with AZT, you would be simultaneously hitting two essential parts of the virus. You'd be simultaneously hitting the protease and also the reverse transcriptase. And it's much less likely that changes in the virus could happen in both of those targets at the same time to allow a virus to escape from both of those hits. So AZT combined with these protease inhibitors started to be used around 1997, and it had a huge impact. So on that right-hand graph, you can see this was in the United States, data from the Center for Disease Control. And you can see incidents of different diseases per hundred cases per 100,000 population between 1987 and 2004. And you can see most of these lines for cancer, for stroke, for heart disease, are flat. But if you look at that red line for AIDS, you can see it growing and growing and growing until 1997, when these protease inhibitors started to be used. And then you can see the instance of AIDS plummet. Because these protease inhibitors, combined with AZT, really transformed the ability to treat AIDS patients. Meaning the life expectancy went from maybe 18 months up to 30 years. So how have how have can how has continued development taken place? Of course, researchers haven't rested with these medicines from the 1990s. There are new medicines which target the reverse transcriptase, which are better than AZT, which have fewer side effects and are less likely to be susceptible to resistance. There are inhibitors which target the integrase as well, that molecule which inserts the viral DNA into the DNA of the cell. And these medicines are combined. So people who are HIV positive will probably be taking one of these drugs in this country. And these will contain one or two integrase inhibitors mixed with one or two reverse transcriptase inhibitors. And these medicines have been truly transformative. As I said, people taking these pills daily are able to maintain the load of virus in their body to undetectable levels. They don't suffer any symptoms of the disease and they can't transmit the disease either. Other developments are the production of injectable forms of these medicines. So rather than a daily pill, for people for whom that is challenging to take a daily pill, they're injectable forms where an injection may last uh one or two months instead, making it easier for groups of people to comply with taking these medicines. And uh lastly, um now that we have enough of these medicines that they're not, they don't each have to be frontline therapy for people who are infected with HIV, they can also be used prophylactically. So it's these same cocktails of medicines hitting these same targets, the integrase, the reverse transcriptase, usually. It's these cocktails, same cocktails of similar molecules targeting these same combinations, which can be used prophylactically as part of a again a daily pill, meaning that people are much less likely to catch the HIV infection. Um and uh and these these these um these PrEP tablets are uh very effective. They're about 99% um effective. So um that means 99 times less likely, if exposed to uh the virus, um, to uh receive an infection. And also longer-lasting um injectable uh forms of prophylaxis are also starting to become available. Um and one of them is this molecule called Lanacapavia, which is a new class of drug which actually targets the capsid. So I've described this bullet-shaped capsid at the core of the HIV virus a number of times. Um and in the middle there you can see that this this architecture is this beautiful structure made of these hexagonal um building blocks or tiles, which creates these architectures. And Lena Kapavia binds to these and stops that capsid from forming properly. You can see in the electromicrograph on the left that the capsid is all a bit wobbly in that particular virus that's been treated with this medicine. So, is the HIV pandemic over? Um, we've seen that this was a horrific disease. Um, we've seen uh what it was like to have AIDS in the 1980s, and we've also seen the transformative effect of understanding the virus and developing these new medications. So, is is the pandemic over? Uh sadly, it is not. Um, so these are numbers uh from the World Health Organization for 2025. So um they estimate that around 41 million people are currently living with HIV infection, um, and that was a 1.2 million uh additional infections in 2025. Um, and tragically it's still uh 570,000 people uh died of AIDS um in 2025. So um I've talked about um AIDS and HIV from a very British and American perspective, but of course that's not the AIDS pandemic that that we we know today. Um this is data from the Lancet in 2024, um, and the top graph shows HIV incidents, and the bottom graph shows HIV deaths with yellows, oranges, and reds uh being the greatest prevalence. So those 41 million HIV-positive people, 26 million of them are in Africa, um, and more than half of the HIV deaths are in Africa. So why is this? Why are people still getting infected? And why are people still tragically dying of AIDS when we have medicines which can uh cure keep the virus at undetectable levels? Well, there are a number of reasons. Firstly, the WHO estimate that 88% of people who are HIV positive know that they are, which means that 12% don't know that they are. With a 10 to 15 year period of latency where the virus hides uh within our cells, um, these people are at risk of unknowingly transmitting the virus uh to partners or uh to an unborn child, for example. So that's five million people who don't know that they have malaria who are creating this risk. Um also um it's not possible currently to cure somebody from having an HIV infection. And what I mean by that is that we can't eradicate the virus from somebody's body at the moment. So if somebody stops taking their ART medicines, um, the virus can emerge. It's undetectable, it's untransmittable, but it's still there inside their immune cells, inside these CD4T cells. And these medicines, which are taken daily or through an injection, are keeping it at bay. They're meaning that if it starts to emerge from its latent form, it can't replicate, it can't cause us to be ill, it can't be transmitted. But it is still present. Um, and um, the World Economic Forum estimate that 1.5 million people in Africa live more than an hour's drive from the place that they would be able to collect their ART. And there are growing challenges in the distribution of these medicines as well. So the United States used to be a major provider of ART medicines. And with the cuts to USAID in recent years, uh, clinics have been closing and people have not been getting their medicines. And the WHAO estimates that if if those cuts remain in place until 2029, that will be 6.6 million more AIDS in HIV infections that will take place that would not have taken place had though that USAID uh support uh still been in place. So these drugs are uh are extraordinary, and for those of us uh lucky enough to live in a country or an environment where where those drugs are freely available to us, um we can control those anybody with an HIV infection can control it and live a normal life. Um, but in many areas of the world there are huge challenges in getting those medicines to people and in controlling the infection and in controlling the disease. So, what are scientists trying to do about that? To to make something that's better than these protease inhibitors or these these uh anti these anti-retroviral therapies? Well, there are two approaches. One is protection and one is cure. So the first is is a vaccine. There is still no effective um there's still no effective uh vaccine against HIV. And this is not through want of trying. Researchers started trying to develop uh an AIDS vaccine, an HIV vaccine, as soon as the virus was discovered, as soon as they knew uh what the cause was. So why has it been so hard? Uh the graph on the on the left, um, the top left there sh represents the amount of mutation that happens in an influenza season across the entire globe. So the size of those lines represents the amount of variation you get in an entire influenza season. The bottom left represents the amount of variation you get in a single person infected with HIV. In other words, uh the amount of change that one the HIV virus goes through, the mutation that it goes through in one infected person, is about the same as the entire global influenza uh mutation within a year. And that big graph on the right shows the amount of variation in HIV in an outbreak in the Democratic Republic of Congo. So this virus is hugely mutatable. And it's hugely mutatable because the reverse transcriptase is quite a bad enzyme at copying RNA into DNA. It makes lots of mistakes, and that means that this virus evolves really fast. The second, uh, the right-hand side shows the envelope protein, the protein which coats the surface of the virus particles, and which is the thing which recognizes our immune cells and helps the virus to get inside them. And in blue, there you can see sugary molecules called carbohydrates, which cover the surface of this virus part protein, and that makes it really slippery in molecular terms. It makes it really hard for antibodies to recognize the virus protein. So this combination of a high mutation rate and this flexibility means that the virus is really hard to stop with antibodies. And that's why it's been so hard to make a vaccine. Um, so what are what are the approaches which are being used? Well, probably the most um uh promising approach um has relied on the fact that uh and a few individuals have been discovered in the United States who have antibodies within their blood, and they they were infected with HIV, and they have antibodies within their blood which are able to recognize this envelope protein, and which are and that they're able to recognize it despite all of this world of mutation. The problem is that these are antibodies are really rare, and the reason they're rare is because within our bodies we have the precursor molecules to antibodies, and the precursor molecules that we have in our bodies to antibodies uh to antibodies, they get triggered to mutate by an infection, and they mutate and they change and they develop, and that allows our body to learn to recognize that infectious agent. But these antibodies that can recognize all of these variant HIV viruses are quite very different from the precursor antibodies that we have in our body naturally. So it requires a complex process of sequential mutation to get from what we naturally have in our immune systems to these rare antibodies. So the vaccination strategies that are being tested at the moment and seem to have promise require a number of different vaccines. Each vaccine trains the body to make slightly different antibodies. So what you see on the right hand side is where we want to get to, these really unusual rare antibodies. And on the left hand side, you can see the cells in our body which produce antibodies normally, which look nothing like the antibodies we want except in rare people. And so the plan is to immunize people with a sequence of viruses, vaccines, which get closer and closer to the vaccine which will induce these desirable antibodies. In other words, training the immune system through a series of steps to get from an antibody which doesn't look much like what we want to one which looks a little bit more like it, to one which looks a little bit more like it, and then finally to the antibodies that will be protective. So these sequential vaccinations with slightly different vaccines leading the immune system in the right direction. So these uh these uh vaccines are in development, they're in testing, um, and um there's a lot of enthusiasm and optimism about them, but also they're challenging vaccines to administer because it requires in an African healthcare setting to be able to give people sequential vaccines, each of a different nature, each after a defined period of time. The other opportunity, the other quest is to develop a cure. So, has anybody ever been cured from having HIV? Well, yes, a handful of people have. So on the right, you can see one of them, the first person to ever be cured from having HIV. Um, he's called Timothy Ray Brown, um, but up to the point that he decided to reveal his identity, he was called the Berlin patient. He was diagnosed HIV positive as a student in Berlin in 1995, and he received ART therapy in the mid-90s and was able to live a normal, healthy life. But then 10 years later, um, lightning struck twice and he was diagnosed with leukemia of the blood, another life-threatening condition, and chemotherapy didn't work. So his doctor recommended a stem cell transplant to him. A stem cell transplant will wipe out the blood cells and replace them with um stem cells uh from another donor, from a donor, which will then replace their blood cells. Uh, Timothy Ray Brown had a very clever doctor. Um, his doctor, um Giro Hutter, um in Berlin, um, noted that 1% of Europeans have a mutation in their CD4 plus T cells, which means that they don't have this CCR5 receptor. And that CCR5 receptor is used by the HIV virus to get inside the cells. So, what his doctor decided to do was find a donor of stem cells which lacked this particular receptor and use it to conduct this transplant. And Timothy agreed to this. He had his transplant. Um, this is not uh a simple procedure. It involves having your your immune cells and your the stem cells that produced your blood cells destroyed. It involves uh immunosuppressive medication, it involves a big operation, but it worked. Um, it uh cured his leukemia, and it also meant that the virus couldn't replicate um in his body anymore. Um so he was able to come off ART therapies, and he was able and and uh he remains with undetectable virus um in his body um subsequently. Um this is this a similar procedure has been used for for three or four other people now, including uh somebody in London, the second person, um, to have this process. Um but it's not something you would choose instead of uh taking ARTs. It's a really challenging process, and it's it's a it's almost a byproduct of leukemia treatment. But um, can scientists develop other ways of achieving a similar sort of outcome? Um, and these are all things which are sort of underway at the moment and and and um very active research areas, um, a variety of different ways in which uh researchers are trying to get rid of the latent virus, whether it's to use, you may have heard of CRISPR, which are agents which can cut bits of DNA out of uh larger pieces of DNA. So people are uh working on developing methods to cut the virus out of our cells using these CRISPR processes. They're also developing ways to trigger the virus to emerge from its latent state, hidden uh within the CD4T cells, to kick it out of latency. So all of the viruses in somebody's body simultaneously emerge from their CD4T cells in the presence of ARTs, which would then prevent them from replicating. Or causing people to produce these rare antibodies that will prevent them from getting protect them from HIV, uh, similarly by a gene therapy delivery method. So there are lots of different approaches being trialed and tested at the moment and at different stages in the trial process. So none of these are licensed yet. But the hope is in in years to come it might be possible uh to uh not just control uh the HIV uh virus in our bodies, admittedly, control it really well so that way that people live normal life expectancies, but to actually eradicate it from people's bodies in in a true uh cure and therapy. So is the HIV pandemic over? Um well I told you some Stark stories at the beginning about HIV in the 1980s, and um the transformative effect of these ARTs means that for people who have access to them, um being HIV positive um one can live a normal life expectancy, well, HIV positive, um, a normal healthy life with no risk of transmitting the virus. And prophylaxis uh can also help people to prevent themselves from being infected. Um, but HIV infection is currently for life with no uh cure other than um rather dramatic ones such as stem cell transplants. And because access to ARTs and PrEP is limiting, HIV remains a huge problem. The pandemic is not over. And as well as uh working out how to distribute these medicines uh more fairly and more globally, um, we also need to work on new uh ways to really uh eradicate HIV and also to prevent uh people from catching it. So, yeah, that's all I wanted to tell you about today. Hopefully, you've enjoyed this uh story of scientific triumphs over a horrible disease, uh, but one in which we have um still much work to do, and thank you for listening.