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These 4 promising breakthroughs are bringing HIV researchers closer to a cure
Photo #8679 February 03 2026, 08:15

Nearly 45 years after the first HIV diagnosis, science is closer than ever to a cure for the virus that causes AIDS — but we’re not there yet, researchers say.

While perhaps a dozen people worldwide have been declared free of the virus, those results haven’t been replicated widely, and treatments for some involve continuing therapies or procedures, like stem cell and bone marrow transplants, that aren’t feasible for widespread use.

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So far, there is no “magic bullet” to cure HIV for good. But scientists are making rapid progress on several fronts and say a cure is within reach. Here’s a roundup of where the latest progress stands.

A golden “supertherapy” that gives HIV a one-two punch

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A study from the Federal University of São Paulo (UNIFESP), published in August, details how a team of researchers in Brazil succeeded in eliminating HIV from a patient’s body for 78 consecutive weeks with a “supertherapy”, achieving the result with a combination of medications alone and without stem cell transplants or gene therapy.

The study combined potent antiretroviral drugs with innovative compounds including auranofin, a gold salt, that were designed to both activate and eliminate viral reservoirs of HIV while also stimulating the immune system to destroy infected cells in a one-two punch at the virus.

“The patient benefits not only from drug treatment but also from the ability to reduce the viral load to the lowest possible level. The lower the viral load, the closer the patient gets to a cure,” lead investigator Ricardo Sobhie Diaz, director of the Retrovirology Laboratory at UNIFESP told Medscape.

Self-replicating “Stemmy” CD8 cells could help defeat the virus

While now-common antiviral drugs (AVRs) knock back levels of HIV in both blood and tissues, they don’t overcome one major obstacle for an HIV cure: The stubborn “reservoirs” of cells that harbor dormant viral DNA in the body. When people stop taking the drugs, the virus almost always resurges within weeks.

In two independent studies at the University of California at San Francisco and the Ragon Institute of Mass General Brigham, researchers from the Massachusetts Institute of Technology (MIT) and Harvard zeroed in on a class of white blood cells known as memory T cells, studded with CD8 receptors, structures on the cellular surface that are essential to immune defense.

Both studies found that precursors to these “killer T cells” are strongly tied to long-term control of HIV after treatment was stopped in some study participants. The precursors have a stem cell–like quality, and they more readily made copies of themselves when the virus started to return.

Stimulating the production of these “stemmy” CD8 cells “might be the key to getting control [over HIV] in more than the small percentage of people who are currently achieving it,” the Ragon Institute’s David Collins told Science magazine.

Steve Deeks, co-leader of the UCSF study, said those cells “may be the magical biomarker we need for a cure.”

A 3D medical illustration showing an HIV retrovirus targeting T-cells.
A 3D medical illustration showing an HIV retrovirus targeting T-cells. | Shutterstock

A “kick and kill” strategy that may have actually cured one woman

A years-long study in Rwanda has yielded promising results with a strategy that researchers call “kick and kill.”

“HIV doesn’t live in our blood, it lives in reservoirs, whether in the lymph nodes or the liver or the brain, so you need to kick it out” in order to kill it, Krista Dong, an assistant professor also with the Ragon Institute, told NPR in August.

In the study, 20 young women on antiviral therapy for an average of seven years were asked to pause the drugs, allowing the HIV lurking in those reservoirs to emerge.

Researchers flushed it out of hiding with a unique drug called vesatolimod, followed a week later by a one-time infusion of broadly neutralizing antibodies (bNAbs). Those antibodies were predicted to bind to the virus and summon immune cells to eliminate it.

By trial’s end, four women remained in remission. One would later experience a viral rebound, while two resumed AVR’s, one to ensure a safe pregnancy and the other because a new job precluded her ability to receive regular monitoring.

More than two years after stopping medication, one woman remains HIV-free and off treatment. She could be cured.

“Novel vaccines” can train the immune system to kill HIV

In tandem with research on a cure for HIV, an HIV vaccine is a priority for scientists. So-called “novel vaccines” are key to that effort.

Two research teams reported in May that HIV vaccine approaches — aimed at training the immune system to produce specialized antibodies against the virus — have taken steps forward, POZ magazine reports.

Both studies showed that different engineered immunogens — substances that trigger a specific immune response in the body — could inspire production of precursor immune cells with the potential to produce those same broadly neutralizing antibodies (bnAbs) introduced in the Rwanda study to kill off diverse strains of HIV.

“We’ve now shown in humans that we can initiate the desired immune response with one shot and then drive the response further forward with a different second shot,” William Schief, PhD, of Scripps Research, said of the institute’s study of 18 participants in South Africa and Rwanda. “These trials provide proof of concept for a stepwise approach to elicit custom-tailored responses — not just for our vaccine but for the vaccine field at large, including non-HIV vaccines.”

That second shot, or boosting strategy, is designed to guide the immune response along the path toward bnAb production. All those who received both the primer and booster ended up developing antibody responses — most showed “elite” responses with multiple mutations linked to bnAb development.

“What really surprised us was the quality of the immune response we saw after just two shots,” Schief said. “We didn’t anticipate it would be that favorable.”

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