2025-08-15 22:00:00
Beyond brains, robots desperately need smarter bodies.
Watch Boston Dynamics’ Atlas robot doing training routines, or the latest humanoids from Figure loading a washing machine, and it’s easy to believe the robot revolution is here. From the outside, it seems the only remaining challenge is perfecting the AI (artificial intelligence) software to enable these machines to handle real-life environments.
But the industry’s biggest players know there is a deeper problem. In a recent call for research partnerships, Sony’s robotics division highlighted a core issue holding back its own machines.
It noted that today’s humanoid and animal-mimicking robots have a “limited number of joints,” which creates a “disparity between their movements and those of the subjects they imitate, significantly diminishing their … value.” Sony is calling for new “flexible structural mechanisms”—in essence, smarter physical bodies—to create the dynamic motion that is currently missing.
The core issue is that humanoid robots tend to be designed around software that controls everything centrally. This “brain-first” approach results in physically unnatural machines. An athlete moves with grace and efficiency because their body is a symphony of compliant joints, flexible spines, and spring-like tendons. A humanoid robot, by contrast, is a rigid assembly of metal and motors, connected by joints with limited degrees of freedom.
To fight their bodies’ weight and inertia, robots have to make millions of tiny, power-hungry corrections every second just to avoid toppling over. As a result, even the most advanced humanoids can only work for a few hours before their batteries are exhausted.
To put this in perspective, Tesla’s Optimus robot consumes around 500 watts of power per second for a simple walk. A human accomplishes a more demanding brisk walk using only around 310 watts per second. The robot is therefore burning nearly 45 percent more energy to accomplish a simpler task, which is a considerable inefficiency.
So, does this mean the entire industry is on the wrong path? When it comes to their core approach, yes. Unnatural bodies demand a supercomputer brain and an army of powerful actuators, which in turn make robots heavier and thirstier for energy, deepening the very problem they aim to solve. The progress in AI might be breathtaking, but it leads to diminishing returns.
Tesla’s Optimus, for instance, is smart enough to fold a t-shirt. Yet the demonstration actually reveals its physical weakness. A human can fold a t-shirt without really looking, using their sense of touch to feel the fabric and guide their movements.
Optimus, with its relatively rigid, sensor-poor hands, relies on its powerful vision and AI brain to meticulously plan every tiny motion. It would likely be defeated by a crumpled shirt on a messy bed because its body lacks the physical intelligence to adapt to the unpredictable state of the real world.
Boston Dynamics’ new, all-electric Atlas is even more impressive, with a range of motion that seems almost alien. But what the viral acrobatics videos don’t show is what it can’t do. It could not walk confidently across a mossy rock, for instance, because its feet cannot feel the surface to conform to it. It could not push its way through a dense thicket of branches, because its body cannot yield and then spring back.
This is why, despite years of development, these robots mostly remain research platforms, not commercial products.
Why aren’t the industry’s leaders already pursuing this different philosophy? One likely reason is that today’s top robotics firms are fundamentally software and AI companies, whose expertise lies in solving problems with computation. Their global supply chain is optimized to support this with high-precision motors, sensors, and processors.
Building physically intelligent robot bodies requires a different manufacturing ecosystem, rooted in advanced materials and biomechanics, which is not yet mature enough to operate at scale. When a robot’s hardware already looks so impressive, it’s tempting to believe the next software update will solve any remaining issues, rather than undertaking the costly and difficult task of redesigning the body and the supply chain required to build it.
This challenge is the focus of mechanical intelligence (MI), which is being researched by numerous teams of academics around the world, including mine at London South Bank University. It derives from the observation that nature perfected intelligent bodies millions of years ago. These were based on a principle known as morphological computation, meaning bodies can perform complex calculations automatically.
A pine cone’s scales open in dry conditions to release seeds, then close when it’s damp to protect them. This is a purely mechanical response to humidity with no brain or motor involved.
The tendons in the leg of a running hare act like intelligent springs. They passively absorb shock when the foot hits the ground, only to release the energy to make its gait stable and efficient, without requiring so much effort from the muscles.
Think about the human hand. Its soft flesh has the passive intelligence to automatically conform to any object it holds. Our fingertips act like a smart lubricator, adjusting moisture to achieve the perfect level of friction for any given surface.
If these two features were incorporated into an Optimus hand, it would be able to hold objects with a fraction of the force and energy currently required. The skin itself would become the computer.
MI is all about designing a machine’s physical structure to achieve passive automatic adaptation—the ability to respond to the environment without needing active sensors or processors or extra energy.
The solution to the humanoid trap is not to abandon today’s ambitious forms, but to build them according to this different philosophy. When a robot’s body is physically intelligent, its AI brain can focus on what it does best: high-level strategy, learning and interacting with the world in a more meaningful way.
Researchers are already proving the value of this approach. For instance, robots designed with spring-like legs that mimic the energy-storing tendons of a cheetah can run with remarkable efficiency.
My own research group is developing hybrid hinges, among other things. These combine the pinpoint precision and strength of a rigid joint with the adaptive, shock-absorbing properties of a compliant one. For a humanoid robot, this could mean creating a shoulder or knee that moves more like a human’s, unlocking multiple degrees of freedom to achieve complex, life-like motion.
The future of robotics lies not in a battle between hardware and software, but in their synthesis. By embracing MI, we can create a new generation of machines that can finally step confidently out of the lab and into our world.
This article is republished from The Conversation under a Creative Commons license. Read the original article.
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2025-08-14 22:00:00
The first-of-its-kind treatment using donated cells lasted for at least three months and produced insulin.
A new treatment for type 1 diabetes is moving closer to reality.
In late 2024, a 46-year-old Swedish man received 17 injections of a unique pancreatic cell cocktail. The cells, donated from a healthy stranger, had been stripped of two critical genes that trigger immune rejection.
For the next three months, the cells evaded the recipient’s immune system and produced insulin, all without the need for immunosuppressive drugs. Results from the trial, the first of its kind, were published this month in The New England Journal of Medicine.
“It’s a major breakthrough, and it’s remarkable,” Bernhard Hering at the University of Minnesota Twin Cities, who wasn’t involved in the study, told Science.
In type 1 diabetes, the body’s immune system attacks and destroys pancreatic cells that pump out insulin, making it difficult to control blood sugar levels. The disease can be managed with carefully timed insulin injections. But it’s a treatment, not a cure.
“Intensive insulin therapy delays the onset and slows the progression of long-term complications,” and it’s been used for more than 100 years, wrote study author Per‑Ola Carlsson and team at Uppsala University, who collaborated with Sana Biotechnology on the study. But people with type 1 diabetes still have a higher risk of serious heart and blood-vessel problems and a shortened lifespan.
A cure would replace damaged cells with healthy ones. Insulin-producing cells clump together with other pancreatic cells into rounded blobs called islets. These can be isolated and transplanted into people with diabetes—often multiple at a time—as a sort of back-up generator to produce insulin. But the recipient has to take immunosuppressive drugs for life, which dampens their ability to fight off infections and increases the risk of cancer. Cells that evade the immune system could, in theory, provide long-term care and better quality of life.
The immune system is a cellular brigade, effective at fighting off infectious diseases. But it can also become an adversary in transplantation.
Each cell has a unique protein fingerprint on its surface. The immune system recognizes these as either friend—part of the body—or foe. Islet cells from a stranger immediately activate a swarm of immune attacks.
Killer T cells, true to their name, release proteins that tear the transplanted cells apart. B cells churn out a slurry of antibodies that grab onto the transplants and activate a cascade of immune proteins to recruit other cell types, such as macrophages—giant blobs that literally eat up any tagged enemy—and natural killer cells. The latter are immune-system assassins, capable of killing cells that lack normal proteins that would usually mark them as friendly.
The entire immune brigade activates after a transplant and this leads to rejection. Without immunosuppressive drugs, donated islets can’t survive in people with diabetes.
A few years back, the authors of the new study found a way to strip immune-triggering proteins from donated islet cells.
They zeroed in on two major proteins, HLA-I and HLA-II, that dot the cells’ surfaces. Using the gene-editing system, CRISPR, they snipped out genes encoding both proteins. Theoretically, this would protect the cells from immune rejection.
But the strategy is a double-edged sword. The proteins are normal parts of a cell. Getting rid of them causes the immune system to view the engineered cells suspiciously and target them with natural killer cells. So, the team added another protein called CD47. This protein acted like camouflage shielding the cells from the immune brigade.
Tests in diabetic models of mice and a monkey found both incorporated the cells without needing immunosuppressants. Results from the monkey were especially promising. The engrafted cells pumped out enough insulin to sustain the animal’s blood sugar levels for at least six months without the need for additional insulin and no observed side effects.
Encouraged by the results, the team started a clinical trial. They took islets from a 60-year-old donor with the same blood type as the trial recipient and edited them. Not all cells retained the changes. Although nearly all were stripped of immune-triggering HLA proteins, less than half contained the added immune-soothing CD47 protein.
The final product was an amalgamation of cells, each with a different genetic profile. As a safety measure, the team injected a relatively small dose—80 million engineered cells—into the participant’s arm while he was under general anesthesia. He tolerated the therapy well and was released from the hospital the next day.
Over the next three months the team monitored his immune system. Unedited cells provoked a strong but transient T-cell attack, which declined after a week. Meanwhile, cells stripped of both HLAs still caught fire from macrophages—the “cell-eaters”—and natural killer cells.
Cells that had been fully edited, however, escaped the immune onslaught entirely and continued producing insulin for three months. In lab tests, the team “did not detect any immune response targeting” the cells, they wrote.
The volunteer was diagnosed with type 1 diabetes at five years of age. Before the trial, his islets struggled to produce insulin, and he showed signs of an over-zealous immune system.
Following treatment with the engineered cells, however, his insulin levels increased after slurping a smoothy full of fats, protein, and carbohydrates. A follow-up imaging test found the transplanted cells thriving in his forearm muscle. Twelve weeks after injection, the man’s arm had functional islets that could produce insulin—without taking any immune-suppressing drugs.
He experienced some mild side effects, including blood clots in small, surface veins at the site of injections. These can be treated with heat or blood-thinners.
“To my mind this is a huge success,” Carlsson told Science.
The study moves us closer to a cure for diabetes. Compared to the animal studies, the man only received a very small dose (roughly seven percent of the amount used in animals). But his insulin response tracked with predicted outcomes based on previous studies. Upping the number of engineered cells could nix the need for insulin injections.
Other cell therapy efforts for type 1 diabetes are underway. Vertex Pharmaceuticals recently published promising results of a stem-cell-based therapy. The treatment slashed dangerous blood sugar spikes and dips in type 1 diabetic volunteers over the course of a year and without the need for insulin. However, all of them had to take immunosuppressant drugs.
Immune-evading cells have “long been viewed as a holy grail,” wrote the authors.
The team is now exploring ways to engineer insulin-producing cells from stem cells to increase production. They’re also keeping up with the recipient to make sure the transplanted cells continue making insulin and evading immune attacks.
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2025-08-13 03:13:48
The study adds to growing evidence that GLP-1 drugs could offer broad health benefits and potentially help people live longer, healthier lives.
Ozempic has been called a wonder drug for the wide range of ailments it seems able to treat. Now, researchers have found solid evidence it could even slow aging.
Originally designed to treat Type 2 diabetes, Ozempic is the brand name for a molecule called semaglutide. It’s part of a family of drugs known as GLP-1 agonists that also includes Wegovy and Mounjaro. These drugs work by mimicking the natural hormone GLP-1.
GLP-1 has a variety of roles including the regulation of blood sugar by promoting insulin production and inhibiting the release of a hormone called glucagon that increases blood sugar levels. It also helps slows down stomach emptying, which can make you feel full for longer, and activates neurons in the brain that make you feel satiated.
The latter effects are why these drugs are emerging as powerful weight-loss tools. However, there’s growing evidence Ozempic’s potential goes further, with studies showing it could help treat cardiovascular disease, Alzheimer’s, and even substance abuse.
Most tantalizing, however, is the possibility it could act as a broad anti-aging medication. Now, a clinical trial has found the strongest evidence yet that this could be viable. Researchers administered Ozempic to people with a condition that causes accelerated aging. After a 32-week course, those who received the drug were biologically younger by as much as 3.1 years, on average, according to a preprint paper.
“Semaglutide may not only slow the rate of aging, but in some individuals partially reverse it,” Varun Dwaraka, director of research at diagnostics company TruDiagnostic who worked on the trial, told New Scientist.
There was already tentative evidence that GLP-1 drugs could provide broad protection against many of the diseases associated with aging. Last summer, results from a trial on 17,604 overweight people with cardiovascular disease showed that those given Ozempic were less likely to die from any condition rather than just heart disease.
But this latest trial was more directly focused on establishing the anti-aging potential of the drug. It involved 108 patients with HIV-associated lipohypertrophy, which causes abnormal fat accumulation and has been associated with accelerated cellular aging. Half of the participants were given a weekly shot of Ozempic for 32 weeks, while the other half received a placebo.
The researchers then measured each participant’s biological age at the start and end of the trial using an “epigenetic clock.” These tools measure chemical changes to our DNA that build up as we age and alter how different genes are expressed.
On average, the team found that those who had been given Ozempic had epigenetic profiles 3.1 years younger than those who had not received the medication. But interestingly, the impact was not spread evenly across the body. The team found the biggest anti-aging effects in the inflammatory system and brain, where the clock had been dialed back by almost five years.
Dwaraka told New Scientist that the effect probably comes from semaglutide’s anti-inflammatory properties and the reduction of fat—the accumulation of which can cause the release of molecules that accelerate aging—around key organs.
But it’s important to note that there are considerable question marks around how reliably epigenetic clocks measure biological age, with significant discrepancies across different tissue types.
Nonetheless, the study adds to the growing pile of evidence that these GLP-1 drugs provide broad health benefits and could potentially help all kinds of people live longer and healthier lives.
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2025-08-11 23:20:07
Sticky when wet: The glue could seal injuries, heal wounds, and repair ships.
Talk about an unusual sight: A bright yellow rubber ducky stuck to a wet seaside rock. Waves pummel it for days, but it doesn’t move an inch—thanks to an ultra-sticky glue designed by AI.
If you’ve ever tried patching a leaky pipe or roof, you’ll know that chemical glues don’t work well. Super glues rapidly harden with moisture, and there’s very little time to apply them. They also tend to crack on uneven surfaces, like rocks or tubing, and in salty and wet conditions.
Soft hydrogels are a more pliable alternative, but their stretchy properties often directly cancel those that would make them sticky. Still, scientists have long wanted to use hydrogels as glues in medical applications. A super-sticky hydrogel could seal deep wounds, act as a Band-Aid during surgery, and help tissues heal faster. They could also coat prosthetics or wearable biosensors.
The problem? The body tends to be wet, uneven, and salty. Nature has a solution. From bacteria to barnacles, mussels, and snails, a range of creatures squish out tacky protein glues that let them glide, crawl, or grab wet surfaces. These are sometimes so strong you need tools to pry the animals off.
Now, a team from Japan and China has transformed these natural proteins into sticky hydrogels and used AI to dream up even stickier versions. One of the AI’s creations clung to ceramic, glass, and metal surfaces in salt water for over a year—with a kilogram (roughly 2.2 pounds) of weight hanging from it. And yes, it also stuck a rubber ducky to an inhospitable seaside rock. Another sealed off a burst water pipe for five months. Both versions were also biocompatible with mice, suggesting the AI-generated super glues have a future in medicine.
“Super-adhesive hydrogels such as these that stick strongly to irregular and wet surfaces could be transformational for many biomedical applications,” wrote Laura Rosso at University of Milano-Bicocca, who was not involved in the study.
Using AI to discover and design materials isn’t new. But studies have mostly focused on hard materials or small chemicals. One of these found millions of previously unknown crystals that could be useful in microchip and battery designs. Another, combined with a robotic system, automatically synthesized a multitude of new materials.
But ironically, squishy hydrogels have always been a hard nut to crack.
Hard, inorganic materials have well-defined structures and properties, making it easier to train AI to model them. In contrast, hydrogels are made of squishy molecules that swell in water. The gels contain networks of molecules that extend “branches” like tiny trees. The 3D structure of a gel depends on how each molecular branch interacts with the others.
The materials also deform under pressure and swell in wet environments. These properties are the antithesis of what you’d want in a super-sticky glue.
Using AI to find “hydrogels suitable for a specific function is a much more complex task” than discovering hard materials, wrote Russo. AI has only been used to predict how hydrogels behave, such as how they swell and if they’re useful for 3D printing projects. You would need a large database of sticky proteins for AI to learn how to design them—but there isn’t one.
The new study took inspiration from roughly 200 species that pump out sticky proteins, including bacteria and barnacles. Many of these proteins have been sequenced.
Scanning existing protein databases, the team noted which amino acid sequences could lead to proteins that stay sticky under water. They then painstakingly designed and made 180 hydrogels, each built from molecules with the highest chances of acting like natural adhesives. In lab tests, they documented their stickiness, swelling, and how they behaved in running water.
Using this data, the team trained an AI to design more powerful underwater hydrogel glues. They fed the AI’s best results back into the algorithm to improve them further. Three cycles later, the adhesive strength of the top three hydrogels far outperformed the training dataset.
These included R1-Max, the gel that stuck the duck to a rock. A wet, slippery seaside rock is one of the worst scenarios for a glue. Waves can easily peel off a lightweight toy, and tides change the moisture level, which most glues can’t tolerate.
“We want to show our adhesive hydrogel…can glue to the duck on the wet rock…and the duck is cute,” study author Hailong Fan told Nature. Battered by incoming waves, the duck proved stubborn as a barnacle on its rocky perch.
In another test, the hydrogel, shaped like a large Band-Aid, instantly patched a pipe blasting water. The gel sealed the hole for more than five months, suggesting it could be used to fix emergency underwater leaks.
The material is also biocompatible. When inserted under the skin of mice, the critters went on their merry way without notable immune reactions or other side effects. “Super-adhesive hydrogels such as these that stick strongly to irregular and wet surfaces could be transformational for many biomedical applications,” wrote Russo.
The AI could design other soft materials too, especially ones with medical uses. But it will have to navigate the complexities of tissues and organs—a hydrogel designed for the skin may not work on the heart or arteries. Different molecules in each organ could also alter how the gel works.
The team is now trying to pick their AI’s “brain” to find out why R1-Max is so sticky. Knowing the exact reason could lead to even better protein glues.
More broadly, the work “demonstrates that AI is no longer just being tentatively scoped out as a tool for materials science,” wrote Russo. “It has already been adopted to improve and support the design and generation of materials.”
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2025-08-08 22:00:00
Could a pregnancy be conceived and carried safely in space? And what would happen to a baby born far from Earth?
As plans for missions to Mars accelerate, so do questions about how the human body might cope. A return trip to the red planet would give more than enough time for someone to become pregnant and even give birth. But could a pregnancy be conceived and carried safely in space? And what would happen to a baby born far from Earth?
Most of us rarely consider the risks we survived before birth. For instance, about two thirds of human embryos do not live long enough to be born, with most losses happening in the first few weeks after fertilization; often before a person even knows they’re pregnant. These early, unnoticed losses usually happen when an embryo either fails to develop properly or to implant successfully in the wall of the womb.
Pregnancy can be understood as a chain of biological milestones. Each one must happen in the right order and each has a certain chance of success. On Earth, these odds can be estimated using clinical research and biological models. My latest research explores how these same stages might be affected by the extreme conditions of interplanetary space.
Microgravity, the near-weightlessness experienced during spaceflight, would make conception more physically awkward but probably wouldn’t interfere much with staying pregnant once the embryo has implanted.
However, giving birth, and looking after a newborn, would be far more difficult in zero gravity. After all, in space, nothing stays still. Fluids float. So do people. That makes delivering a baby and caring for one a much messier and more complicated process than on Earth, where gravity helps with everything from positioning to feeding.
At the same time, the developing fetus already grows in something like microgravity. It floats in neutrally buoyant amniotic fluid inside the womb, cushioned and suspended. In fact, astronauts train for spacewalks in water tanks designed to mimic weightlessness. In that sense, the womb is already a microgravity simulator.
But gravity is only part of the picture.
Outside Earth’s protective layers, there’s a more dangerous threat: cosmic rays. These are high-energy particles—“stripped-down” or “bare” atomic nuclei—that race through space at nearly the speed of light. They’re atoms that have lost all their electrons, leaving just the dense core of protons and neutrons. When these bare nuclei collide with the human body, they can cause serious cellular damage.
Here on Earth, we’re protected from most cosmic radiation by the planet’s thick atmosphere and, depending on the time of day, tens of thousands to millions of miles of coverage from the Earth’s magnetic field. In space, that shielding disappears.
When a cosmic ray passes through the human body, it may strike an atom, strip its electrons, and smash into its nucleus, knocking out protons and neutrons and leaving behind a different element or isotope. This can cause extremely localized damage—meaning that individual cells, or parts of cells, are destroyed while the rest of the body might remain unaffected. Sometimes the ray passes right through without hitting anything. But if it hits DNA, it can cause mutations that increase the risk of cancer.
Even when cells survive, radiation can trigger inflammatory responses. That means the immune system overreacts, releasing chemicals that can damage healthy tissue and disrupt organ function.
In the first few weeks of pregnancy, embryonic cells are rapidly dividing, moving, and forming early tissues and structures. For development to continue, the embryo must stay viable throughout this delicate process. The first month after fertilization is the most vulnerable time.
A single hit from a high-energy cosmic ray at this stage could be lethal to the embryo. However, the embryo is very small—and cosmic rays, while dangerous, are relatively rare. So a direct hit is unlikely. If it did happen, it would probably result in an unnoticed miscarriage.
As pregnancy progresses, the risks shift. Once the placental circulation—the blood flow system that connects mother and fetus—is fully formed by the end of the first trimester, the fetus and uterus grow rapidly.
That growth presents a larger target. A cosmic ray is now more likely to hit the uterine muscle, which could trigger contractions and potentially cause premature labour. And although neonatal intensive care has improved dramatically, the earlier a baby is born, the higher the risk of complications, particularly in space.
On Earth, pregnancy and childbirth already carry risks. In space, those risks are magnified—but not necessarily prohibitive.
But development doesn’t stop at birth. A baby born in space would continue growing in microgravity, which could interfere with postural reflexes and coordination. These are the instincts that help a baby learn to lift its head, sit up, crawl, and eventually walk: All movements that rely on gravity. Without that sense of “up” and “down,” these abilities might develop in very different ways.
And the radiation risk doesn’t go away. A baby’s brain continues to grow after birth, and prolonged exposure to cosmic rays could cause permanent damage—potentially affecting cognition, memory, behavior, and long-term health.
So, could a baby be born in space?
In theory, yes. But until we can protect embryos from radiation, prevent premature birth, and ensure babies can grow safely in microgravity, space pregnancy remains a high-risk experiment—one we’re not yet ready to try.
This article is republished from The Conversation under a Creative Commons license. Read the original article.
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2025-08-08 00:11:45
In a Phase 1 trial, up to 80 percent of people receiving an mRNA vaccine produced antibodies against HIV.
HIV destroys the immune system from within. Despite decades of research, there still isn’t a vaccine against the virus. The shape-shifting pathogen rapidly adapts to vaccines and renders them useless. And HIV-blocking drugs are expensive to produce, test, and ship, stifling their impact around the world.
But inspired by Covid, two studies are changing the vaccine recipe. The new vaccines include mRNA molecules encoding the protein “stem” of HIV—a part of the virus that doesn’t mutate as fast. Cells produce the protein, and this warns the immune system. When injected into rabbits and monkeys, two versions of the vaccine triggered an antibody avalanche against HIV.
The vaccines were also shown to be safe in an early trial in healthy human volunteers. After three doses several weeks apart, up to 80 percent of the participants produced HIV-blocking antibodies. A few people developed minor but uncomfortable side effects, including hives and rashes, which lasted months or even years in some.
While not yet perfect, the vaccines are relatively easy to distribute and administer. They also shed light on how different versions of the protein impact immunity: A membrane-bound type was especially promising. The results “should assist HIV vaccine development,” wrote study author William Schief and team at the Scripps Research Institute.
HIV has perplexed scientists since it first emerged in the 1980s. After health officials noted a striking rise in pneumonia and cancers in previously healthy young men, labs eventually isolated HIV as the main antagonist.
The virus destroys multiple types of immune cells that protect us from infection. Roughly speaking, we have two main immune warriors: T cells grab onto invading pathogens or cancer cells and wipe them out, while B cells pump out antibodies.
HIV throttles these defense mechanisms, allowing other diseases to thrive. Before the turn of the century, a simple respiratory infection could be lethal to a person with HIV. But thanks to antiviral drugs, AIDS, the disease that HIV causes, is no longer a death sentence. And PrEP was approved as a prophylaxis over a decade ago. In 2025, the FDA approved the first HIV-prevention drug needing only two injections every year. It completely prevented at-risk women in sub-Saharan Africa from infection for up to six months.
Other prevention efforts have borrowed a genetic hack. Some people are genetically resistant to the virus. Transplanting blood stem cells from these people can reproduce their immunity in those already infected. Last year, a 60-year-old man in Germany living with HIV became the seventh person to be free of the virus for almost six years after transplant.
These strategies have weaknesses though. A full stem-cell transplant requires wiping out existing cells, which takes a toll on an already fragile body. A daily pill is more practical, but people need dependable access to a steady supply.
The new studies tap mRNA vaccine technology to build an alternative to existing solutions.
These vaccines encode segments of a pathogen into mRNA molecules and shuttle them into cells. Cells use the mRNA to produce a small piece of the virus, which teaches the immune system to recognize it as an invader. When infected with the real thing—viruses that cause disease—the body produces antibodies to neutralize it. In HIV, this same strategy protects immune cells from being invaded by the virus and keeps our bodies ready for combat.
The HIV virus has a protective enclosure called an envelope, which contains a protein called Env. Some versions of the protein are soluble and drift into the bloodstream. Others are tethered to the virus and cell membrane. Previous HIV vaccine candidates targeted Env’s “stem” with antibodies. The problem is, the stem can be hidden from antibodies inside the viral membrane.
Other candidates engineered mRNA molecules that instructed cells to make two chunks of the Env protein and increase the immune response. In HIV-infected mice, the mRNA vaccine designed to target those bits of Env spurred the production of antibodies.
The two new studies took this a step further. One encoded both soluble and membrane-bound forms of the Env protein. When injected into the leg muscles of rabbits, the animals developed antibodies to the proteins for up to 24 weeks. Of the two, the membrane-bound version far more effective. In monkeys, the vaccine slashed HIV levels for 26 weeks, and boosted the animals’ B cell response. The immune cells also developed a reservoir of “memory” cells that activate in the presence of another HIV infection.
Encouraged by the results, a second team tested both versions of the vaccine in 108 healthy people. The Phase 1 trial mainly studied safety, but it also monitored the antibody response in volunteers aged 18 to 55 across 10 sites in the US.
Each volunteer received three jabs of a single vaccine at different doses. Like the results in rabbits and monkeys, the protein’s membrane-bound version was more efficient and blocked HIV in nearly 80 percent of people. Soluble versions didn’t do as well, with only four percent of participants generating antibodies.
“The difference is pretty striking,” Sharon Lewin, at the Peter Doherty Institute for Infection and Immunity, who wasn’t involved in the study, told Nature.
The vaccine was mostly easy on the body. But roughly 6.5 percent of participants broke out in large rashes regardless of dose, and some of these lingered for years. The response could be due to a combination of HIV infection and mRNA side effects. The teams are still working out the exact mechanism causing the rashes and ways to combat it.
With almost 41 million people living with HIV globally, the side effect is a manageable bump on the road. “The need for an HIV vaccine is high,” Lewin told Nature.
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