WHO unveils the State of the World's Nursing 2025 report on International Nurses Day
Image: File picture: Damaris Helwig
To mark International Nurses Day, the World Health Organisation (WHO), alongside global partners, unveiled the State of the World's Nursing 2025 (SoWN) report.
The report is a comprehensive analysis of the global nursing workforce and its critical role in advancing health systems worldwide.
The launch event spotlighted key findings and policy recommendations from the report, presented by lead author Dr. Carey McCarthy of WHO.
The event featured an international panel of nursing leaders, including report co-chairs Sheila Bonito of the University of the Philippines and Howard Catton of the International Council of Nurses.
They were joined by Jim Campbell, WHO Director of Health Workforce, and Dr. Amelia Latu Afuhaamango Tuipulotu, WHO Chief Nursing Officer, for a global discussion highlighting the importance of the report across diverse health contexts.
Building on the 2020 edition, the 2025 report reflects changes in the global health landscape, addressing new challenges such as increasingly complex disease profiles, greater demand on health systems, and the urgency of aligning with the remaining years of the Sustainable Development Agenda.
The report delivers the most current data on critical areas, including nursing education, employment, migration, regulation, working conditions, and leadership.
It also provides updated estimates and projections on nursing workforce supply and demand through 2030.
In addition to the global launch, national and regional discussions are being held to explore local data and policy implications.
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The report aims to inform and support evidence-based policy decisions, helping countries determine where and how to invest in nursing to strengthen primary healthcare systems and achieve universal health coverage.
The release of SoWN 2025 comes at a pivotal moment, as Member States prepare for the Seventy-eighth World Health Assembly.
There, they will consider extending the Global Strategic Directions for Nursing and Midwifery 2021–2025 to 2030, as recommended by WHO's Executive Board earlier this year.
With validated data and strategic policy options, the State of the World's Nursing 2025 report is set to be a vital tool for governments, planners, and healthcare leaders committed to building resilient and equitable health systems worldwide.
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Daily Maverick
10 hours ago
- Daily Maverick
TB's tight grip: Why this curable disease is so hard to treat
TB can be cured, but ridding the body of the bug often takes many months and usually requires taking four or more medicines. In this special briefing, Spotlight zooms in on what makes the TB bacterium so hard to beat. There are many things we've learned from studying the ancient Egyptians. One especially fascinating discovery was evidence of skeletal deformities in mummies, which serve as silent markers of a tenacious bug still stalking us today: tuberculosis (TB). With about 10.8 million people around the world getting sick with TB in 2023, it remains the leading infectious disease on the planet, according to the World Health Organization (WHO). In just South Africa, it claims more than 50,000 lives a year. In this Spotlight special briefing, we take a closer look at the bacterium that causes TB and why, even now in an era where TB is curable, beating it still requires months of treatment with multiple medicines. Adapted for survival The mystery of TB's staying power starts with the bug itself. As explained by Dr Jennifer Furin, Mycobacterium tuberculosis is well adapted to survive on multiple fronts. Furin is an infectious diseases clinician and medical anthropologist who specialises in TB. First, she explains, there is its size. TB is spread through the air when someone who has the bacterium in their lungs coughs it up. It's then contained in small amounts of fluid called droplet nuclei. This droplet is precisely the right size to hang in the air, allowing TB to survive for hours and even days. These droplets can then be inhaled by other people and are just the right size to travel to their lungs. 'It is really amazing from an evolutionary point of view and would be absolutely fascinating if it did not lead to such a horrible disease,' says Furin. Secondly, the bacteria themselves are well adapted to avoid being killed, sporting a thick, slimy coating called mycolic acid. This coating makes it difficult for drugs or immune system cells to get into the organism to kill it. The bacteria also have some clever ways of getting around the human immune system, which allows them to 'persist in the body for years and years'. Furin says one way it's able to stay in the body for so long is the bacterium's ability to go into a 'metabolically quiet state' when the immune system starts coming after it. In this state, it stops multiplying until the pressure from the immune system quiets down. It is this combination of being able to pass from person to person and lay dormant in the body when challenged by the immune system that enables TB to thrive in humans. How the body fights back Though hard to estimate with great accuracy, it is thought that only in the region of one in 10 people who inhale the TB bacterium and become infected actually fall ill with TB disease. In fact, some people's immune response is so good that even though they've been exposed to TB, there's no evidence that it was ever able to establish an infection in the lungs. For everyone else exposed to TB, one of two things happens. Either the body mounts an immune response that contains and may eventually kill the bug, or the bacteria get past the immune system and cause illness. To make people ill, the bug needs to get past the first line of defence and get a foothold in the lungs. Unfortunately, the antibodies relied on to kill other bacteria or viruses don't work against TB. Instead, Furin explains, special pulmonary macrophages recognise TB as a threat and 'gobbles it inside them'. Macrophages work by 'swallowing' bugs and then neutralising them by 'digesting' them. But the bacterium's thick, slimy mycolic acid layer prevents the macrophages from killing it. The macrophages with the TB inside, along with other essential immune system cells called CD4 and CD8 cells, then signal more macrophages to help out. These cells then work together to build a wall around the bacteria to keep it contained. Furin compares the CD4 and CD8 cells to foremen who oversee the building of a wall called a granuloma, while the macrophages are like the bricks and cement that form the actual structure. This wall around the TB bacteria needs to be constantly maintained by the immune system. If the immune system is weakened, Furin says the walls break down and the bacterium escapes, coming out of its dormant state and starts multiplying again. If this happens, TB could spread beyond the lungs to other parts of the body. If the walls are built right and maintained, then eventually the bacterium is starved to death. Yet, this process can take a long time, sometimes years, because of the bacterium's ability to go dormant. 'Double-edged sword' The 'interaction between TB and the immune system is a double-edged sword', says Professor Graeme Meintjes, an infectious diseases specialist with a research interest in HIV and TB at the University of Cape Town. 'The immune system is trying to contain and kill TB. But at the same time, TB is using the immune system to perpetuate infection from one person to the other,' he says. Meintjes explains that TB has evolved alongside people and developed special proteins and molecules that cause the immune system to react to it. It needs this reaction to cause damage in the lungs, leading to its being released during coughing or even breathing, which helps spread it to other people. 'The TB excites the immune response that causes damage [to the lungs] and that allows it to be released into the airway and either coughed or breathed out. So, there's some evidence that TB has evolved to elicit the immune response in order to achieve that,' he says. Adding to this, for some people cured of TB, Furin says that a condition known as post-TB lung disease can in part be caused by the granulomas grouping together, which causes cavities to form in the lungs. This can lead to scarring and sometimes surgery is required to remove these areas of destroyed lung tissue. The immune system can also start 'over-functioning' if it senses the bacterium has escaped from the granulomas and is spreading. This causes the immune system to send out special chemicals called cytokines that can cause indiscriminate killing of the lung cells around it. She says this is like the immune system going after one target with the intention to kill it, but then blowing up the whole neighbourhood. TB works differently in different people The complex interplay between the immune system and TB makes it difficult to predict which individuals will become sick with TB and who won't, although there are some clear trends. Meintjes says factors like malnutrition, poverty, overcrowded living or working conditions and multiple exposures to TB are some of the biggest drivers of infection and disease. Factors like genetics, the amount of TB someone is exposed to, or a person's initial immune response are also thought to play a role. 'But still, in a given setting where you have two people living in a household, one of them might go on to develop TB disease with the same exposure and the other not. And there are factors that are not fully explained about why some people will develop TB and others won't,' he says. Probably the most important risk factor for TB in South Africa over the past three decades has been untreated HIV. Because HIV targets specifically CD4 cells, it was the worst thing that could have happened in a world with TB, Furin says. HIV infiltrates and kills a person's CD4 cells, which means the immune system then has fewer of the cells ready to fight TB. In 2024, over half (58%) of all adults receiving TB treatment in South Africa were also living with HIV, according to estimates from Thembisa, the leading mathematical model of HIV and TB in the country. Another group that is at high risk of TB disease is children, particularly those younger than two. The good news is that there is a vaccine that reduces this risk. As Furin explains, the BCG (bacillus Calmette-Guérin) vaccine works by showing the CD4 and CD8 cells how to build the 'protective wall' against TB, because the immune systems of children are still too 'immature' to know how to do it without help. 'It [the BCG vaccine] only works for a little bit of time, but it works great to protect kids against those very severe forms of disease, while their own immune systems are learning [how to fight TB],' says Furin. Because the vaccine protects children only for a short time, the WHO recommends that one dose be given at birth for children in countries with a high TB burden. Despite many research efforts to find another vaccine, and a promising candidate being studied in a phase 3 trial, BCG remains the only TB vaccine in use for now. A brief history of TB treatment Though TB has been making humans sick for many centuries, the bug that causes the illness was identified only in 1882, by the German physician and microbiologist Robert Koch. It would be roughly another 60 years before the first effective treatments would become available. Until the 1940s, TB treatment mainly involved staying in a sanatorium. The first drugs to treat TB with any success were the antibiotics streptomycin and para-aminosalicylic acid. These two drugs had significant side effects, and using only two drugs often led to TB becoming resistant to the treatment. As described in this excellent overview, what followed was a 'great flurry of drug discovery research' that lasted from the 1940s to the 1960s. The four drugs used to treat most cases of TB today – isoniazid, rifampicin, pyrazinamide, and ethambutol – were all first used to treat TB in this period. After the 1960s, there was a lull in investment in TB research for several decades, probably because TB rates in wealthy countries had declined, and what cases there were could generally be cured with the new treatments. 'The Global North was very much of the perspective that it's [TB] a disease that's waning and 'it's no longer our problem',' Meintjes says. 'It was seen as a disease of poverty; a disease of other countries, and money was put into diseases that are common in the Global North.' This all changed around the turn of the century with the HIV epidemic and a resurgence of TB, particularly drug-resistant TB (DR-TB) in Europe and North America, says Meintjes. By definition, DR-TB means that some of the standard drugs used to treat TB no longer work. The renewed interest in TB resulted in a new flurry of TB drug discovery. Maybe most notably, in the 2010s, a drug called bedaquiline replaced older DR-TB drugs that were associated with hearing loss. A slightly older antibiotic called linezolid also became a cornerstone of DR-TB treatment. Today, in South Africa, 'normal' drug-susceptible TB (DS-TB) in adults is treated with a six-month treatment course – consisting of four drugs for two months and then two drugs for the next four months. A four-month treatment course has been shown to work in a clinical trial, but is not yet routinely provided in the country. Kids are typically treated for four or six months. DR-TB is treated with anything from three to six drugs, for any time from six to 24 months. How someone's TB is classified is largely determined by which drugs their particular strain of TB is resistant to. Lindsay McKenna, co-director of the TB Project at the Treatment Action Group, suggests thinking of it as a ladder. If the standard four drugs all work for your TB, then you don't have to climb any rungs. If rifampicin doesn't work for you, you have rifampicin-resistant TB (RR-TB) and must climb to the first rung to find drugs that work. If both rifampicin and isoniazid no longer work, you have multi-drug-resistant TB (MDR-TB) and must climb another rung. If you have resistance to even more drugs and you have pre-extensively drug-resistant TB and after that, extensively drug-resistant TB. (In practice, TB programmes often classify RR-TB and MDR-TB together since the same medicines are used to treat them.) All of the above treatments are for people who are ill with TB disease. There is also so-called TB preventive therapy, which aims to kill the TB bacteria in the lungs of someone who is infected, but who hasn't yet become ill with TB disease. These preventive treatments typically involve taking one or two medicines for one to six months, depending on the specific treatment regimen. It is possible that new long-acting formulations could allow for an entire course of preventive therapy to be administered as a single injection, though that research is still at an early stage. How the treatments work One reason for the complexity of TB treatment is the bacterium's large and complex genome. Meintjes says that HIV has nine genes, while TB has around 4,000. Having so many genes means the bug has lots of potential to bypass the effect of drugs targeting certain molecules or pathways and still survive. On the other hand, the many genes, at least in theory, provide many potential targets for antibiotics to attack. As noted, to cure TB, one typically has to attack the bug with at least three or four drugs. Meintjes says it is like a group of lions taking down a large buffalo – each one targeting a different part of the buffalo. Along these lines, TB drugs can broadly fit into different categories based on which part of the bacterium they target. Some drugs attack the way the bacterium builds its cell wall, others disrupt how the bug makes its protein, yet others interfere with how the bacterium produces or gets energy, and finally, some sabotage the way TB replicates. As Meintjes explains, isoniazid targets the cell wall of the bacterium by affecting the formation of molecules within the wall, ultimately causing it to leak and die. Rifampicin targets the genetic mechanisms of the TB bacterium, which prevents it from replicating. Bedaquiline works by targeting the mechanisms that allow the bug to metabolise energy, essentially starving it of fuel. A class of antibiotics called fluoroquinolones, specifically levofloxacin and moxifloxacin, target the TB bacteria's DNA while it's trying to copy itself and stops that process, explains Furin. Another drug, linezolid, interferes with how the bacterium makes proteins, which it needs to survive. It is not entirely clear how some other drugs, like clofazimine and pyrazinamide, work, says Furin. Even when attacking TB with several drugs and from multiple angles like this, it can still take months for all the bacteria in someone's body to be killed and for them to be cured. This is because, according to Furin, sometimes the protective wall formed by the immune system to contain the TB becomes too thick for the drugs to get through. And the environment inside the wall is often very acidic and deactivates some of the drugs that do manage to get in. How treatment could improve Novelist George Orwell, who was diagnosed with TB in 1947, was one of the first people to be treated with streptomycin. 'I am a lot better, but I had a bad fortnight with the secondary effects of the streptomycin. I suppose with all these drugs it's rather a case of sinking the ship to get rid of the rats,' he wrote in a letter at the time. More than 75 years later, TB treatments have improved massively, but drug side effects remain a real problem, especially when treating DR-TB. Some older treatments for TB involved injections of toxic drugs and had horrible side effects, including hearing loss and kidney damage. While newer drugs are better, there are still issues. Linezolid, for example, can cause peripheral neuropathy (painful tingling in the hands and feet) and anaemia. McKenna says none of the TB drugs is 'necessarily a walk in the park' and all come with side effects. This is because of the drugs themselves, the dosages required to kill the TB bacterium, and how long the drugs need to be taken. Because of this, much of the focus in TB research has been on finding drug combinations that can reduce the duration of treatment and the severity of side effects. For Furin, an ideal future regimen includes 'fewer pills' – she's hoping for one pill once a day for no more than eight weeks, 'fewer side effects', and doing away with the one-size-fits-all approach. Her reference to the 'one size fits all approach' points to one of the central tensions in TB treatment programmes. People with TB often do not get optimal treatment based on the specific characteristics of their own illness. For example, in countries with limited testing for drug resistance, people might be treated with medicines that their specific strain of TB is resistant to. They might thus suffer the side effects of that medicine without any of its benefits. This is less of an issue in South Africa than elsewhere, since the country's health system provides routine testing for resistance against several of the most important TB drugs. There are also questions about whether everyone really needs to be treated for six months to be cured. A landmark study called Truncate has shown that many people can be cured in two months. The difficulty is that we can't currently predict who will be cured after two months and who will need the full six months, or even longer. Figuring this out, as McKenna points out, would enable more personalised care that would mean fewer people are over- or under-treated. Some in the TB world have argued for the development of a pan-TB regimen – a combination of three or so drugs that nobody is resistant to and that accordingly could be given to everyone with TB, no matter what strain of TB they have. The benefit of such a pan-TB regimen would be that it would dramatically simplify the treatment of TB if it worked. But the experts interviewed by Spotlight agree that resistance is likely to develop against the drugs in such a regimen, and as such, testing people for drug resistance will remain necessary, as will alternative treatment regimens. Furin also points out that pharmaceutical companies have a greater incentive to invest in a pan-TB regimen since its potential market share is bigger than for drugs in a more fragmented treatment model. A hard task, getting harder One of the biggest obstacles in the way of finding new TB treatments is that there really aren't any reliable shortcuts when it comes to doing the research. With HIV, one can get a good idea as to whether a treatment is working by looking at biomarkers such as a person's viral load and CD4 count. TB, by contrast, doesn't have any similarly clear biomarkers that tell us whether a treatment is working or not. Arguably, the most promising biomarker for TB is bacterial load – essentially, how many bacteria are left in someone's sputum a while after treatment has begun. Having a high TB bacterial load is associated with a poor treatment outcome, but the problem is that it is difficult to measure reliably. Without a good biomarker, the only way to measure how well treatment is working is to follow patients for a long time and see if they are cured, and if they are, whether they suffer a relapse. Because of this, TB treatment trials often take several years to complete. Despite these challenges, there has been a good deal of activity in recent years. 'There are about 20 different new drugs in clinical trials at the moment – either early or later phase,' says Meintjes. But much of that momentum might now be lost because of the United States' abrupt slashing of research funding, including much TB research. The US government has until now been the largest funder of TB research by some distance. It spent $476-million or over R8.7-billion through its agencies on TB research in 2023, according to a report by TAG. Many ongoing US-funded TB clinical trials have already been affected, according to McKenna, although there have recently been indications that some research funding might be restored. Where does this leave us? That most people with TB can be cured is something worth celebrating. That treatment for DR-TB has become a lot better and shorter over the past two decades is also something to be grateful for. But as we have shown in this Spotlight special briefing, TB is a tough and ancient adversary and keeps adapting. The treatments at our disposal today are far from as good as we'd like them to be. The treatment side effects are often horrible, and many people find it very hard to take these drugs for month after month. We didn't linger on it, but many people who are cured struggle with post-TB lung disease for the rest of their lives – meaning the bug might be gone, but that person's lungs are never the same again. The scientific search for better TB treatments is not a matter of convenience. It is critical to reducing the suffering that several million people will endure just this year. It is also vital for reducing the number of lives that are still being claimed by this age-old disease. And of course, TB will keep mutating, and we will likely see more and more resistance developing against the drugs that we are depending on today. That is why it is imperative that governments, donors, and pharmaceutical companies all maintain and increase their investment in the search for better TB treatments. After all, TB claims more lives than any other single infectious agent on the planet. If that alone doesn't warrant more investment, what does? But there is also a case to be made that we should change the way we conduct TB research. Ideally, more research should be driven, and informed by, what actually matters to people with TB and to people in the communities where TB is rampant. After all, when given the choice, who wouldn't opt for more personalised and more respectful treatment and care? 'The TB community keeps making the same mistakes over and over and then acts mystified when things do not turn out the way they want,' says Furin. 'All the new drugs and new regimens in the world will never be enough if we do not listen to what impacted communities need, and follow their lead.' DM Additional reporting by Marcus Low.
TimesLIVE
16 hours ago
- TimesLIVE
Making diphtheria great again? Why SA's public health experts are worried about RFK Jr
They used to call it the strangling angel. The grey membrane would take the form of wings at the back of the child's throat, spreading quickly, thickening up like leather. As the diphtheria moved through the body, a toxin would be released, potent enough to stop the heart and paralyse the nervous system. Some of the children who caught it would die within days, their narrow airways blocked by the winged formation. Before vaccines were widely available, diphtheria was a leading global killer. But after the World Health Organisation (WHO) rolled out standard immunisation campaigns in 1974, new cases of diphtheria reduced by more than 90%. Today, most people would be hard-pressed to tell you what diphtheria is, never mind what it does to the body of a small child. But one three-minute video released on social media at the end of June may change all that. That's when US health czar Robert F Kennedy Jr accused Gavi, the international vaccine alliance, of distributing a version of what's known as DTP — the combined diphtheria, tetanus and pertussis (whooping cough) vaccine — that does more harm than good. Kennedy, known as RFK Jr, also halted all US funding to the group until it embraces what he defines as proper science. RFK Jr's vaccine stance is completely at odds with the global public health community and years of science, ignoring years of research that have found vaccines are safe and effective and which have saved an estimated 154-million lives — mostly under the age of 5 — over the past 50 years.
IOL News
19 hours ago
- IOL News
WHO announces lenacapavir as a groundbreaking HIV prevention method
WHO announced a groundbreaking HIV preventative measure Image: Supplied The World Health Organization (WHO) announced a landmark policy at the 13th International AIDS Society Conference (IAS 2025) on HIV Science in Kigali, Rwanda, releasing new guidelines that recommend injectable lenacapavir (LEN) as a twice-yearly pre-exposure prophylaxis (PrEP) option for HIV prevention. This development has the potential to significantly reshape the global HIV response. LEN is the first twice-yearly injectable PrEP product, offering a highly effective, long-acting alternative to daily oral pills and shorter-acting prevention methods. With just two doses a year, LEN marks a transformative step in HIV prevention, particularly for individuals who face challenges with daily adherence, stigma, or limited access to health care. 'While an HIV vaccine remains elusive, lenacapavir is the next best thing: a long-acting antiretroviral shown in trials to prevent almost all HIV infections among those at risk," said Dr Tedros Adhanom Ghebreyesus, WHO Director-General. 'The launch of WHO's new guidelines, alongside the FDA's recent approval, marks a critical step forward in expanding access to this powerful tool. WHO is committed to working with countries and partners to ensure this innovation reaches communities as quickly and safely as possible.' The new guidelines come at a pivotal time, as global HIV prevention efforts have stalled, with 1.3 million new infections recorded in 2024. Key and priority populations — including sex workers, men who have sex with men, transgender individuals, people who inject drugs, those in prisons, as well as children and adolescents — continue to be disproportionately affected. WHO's endorsement of LEN marks a significant step toward broadening and diversifying HIV prevention strategies, empowering people with more choices to protect their health in ways that align with their needs and circumstances. WHO has recommended a simpler, more accessible approach to HIV testing using rapid tests to support the rollout of long-acting injectable PrEP like LEN and CAB-LA. This change removes a major barrier by cutting out complex, expensive procedures and allowing delivery through local clinics, pharmacies, and tele-health. LEN now joins other WHO-approved HIV prevention options — including daily oral PrEP, injectable cabotegravir, and the dapivirine vaginal ring. Although access to LEN outside clinical trials is still limited, WHO is calling on governments and health partners to begin implementing it within national HIV prevention programmes while gathering data on its real-world use and impact. For the first time, WHO now recommends long-acting injectable cabotegravir and rilpivirine (CAB/RPV) as an option for adults and adolescents who are already virally suppressed on oral antiretroviral therapy (ART) and don't have hepatitis B. This is especially helpful for people who struggle with daily pill-taking. WHO also updated its guidance on integrating HIV care with other health services, such as treating high blood pressure, diabetes, mental health conditions (like depression, anxiety, and alcohol use disorders), and improving ART adherence. The organisation now recommends STI screening (gonorrhoea and chlamydia) for key and priority populations, even when no symptoms are present. For people living with HIV who have or are at risk of mpox (formerly monkeypox), WHO strongly recommends starting ART quickly, especially if they've never started treatment or have had long interruptions. HIV and syphilis testing is also advised for anyone with suspected or confirmed mpox. Given funding challenges facing global HIV programmes, WHO released new guidance to help countries maintain essential HIV services. This includes advice on how to prioritise services, manage risks, and keep health systems resilient. Dr Meg Doherty, WHO's HIV programme director, emphasised the urgency of acting on these guidelines: 'We have the tools and the knowledge to end AIDS as a public health problem. What we need now is bold implementation of these recommendations, grounded in equity and powered by communities.' HIV continues to be a major public health issue, with an estimated 40.8 million people living with the virus globally by the end of 2024. While treatment access is growing — 31.6 million people are now on ART — new infections and deaths remain high, particularly in the WHO African Region. With these updated guidelines, WHO said it is offering countries practical tools to make HIV responses more efficient, equitable, and sustainable. The focus now shifts to putting these strategies into action. [email protected] Weekend Argus
