A 63-year-old man in Norway has achieved what researchers describe as a functional cure of HIV, five years after receiving a stem cell transplant from his brother to treat an unrelated blood disorder.
Known in medical literature as the "Oslo patient," the man was treated for myelodysplastic syndrome using allogeneic hematopoietic stem cell transplantation. Researchers confirmed his HIV remission by testing blood, gut, and bone marrow samples, none of which showed any detectable viral reservoirs. The case was published in a peer-reviewed journal and reported by Healthline.
He is the tenth person globally documented to have achieved long-term HIV remission following this type of transplant. Previous cases include the "Berlin patient," the "London patient," and several others identified in the years since. Each case is distinct, but together they are helping scientists build a clearer picture of what conditions allow HIV to be eliminated from the body.
The brother who donated the stem cells carried the CCR5 delta-32 mutation, a rare genetic variant that confers strong resistance to HIV-1, the predominant form of the virus. HIV typically enters immune cells by binding to CCR5 receptors. The mutation prevents those receptors from forming on the cell surface, effectively closing the door the virus uses to establish infection. Most of the ten documented remission cases have involved donors carrying this mutation.
But the mutation alone does not explain every outcome. Researchers note that immune responses and ongoing antiretroviral medication also appear to play a role in clearing what are called viral reservoirs, the hidden pockets of dormant HIV that standard treatment cannot reach and that make a conventional cure so difficult to achieve.
Steven Deeks, a professor of medicine at UCSF who was not involved in the study, described the accumulating cases as a step forward. "There have now been 10 successful transplants," he said. "Each is unique, but they collectively show" progress in understanding HIV remission.
The finding does not point toward a broadly available cure. Stem cell transplants are high-risk procedures typically reserved for patients who already need them to treat cancer or other serious blood disorders. Finding a donor with the CCR5 delta-32 mutation is rare under normal circumstances, and the procedure itself carries significant risks including graft-versus-host disease.
What the Oslo case and others like it do offer is a detailed biological blueprint. Scientists studying these patients are trying to understand precisely which combination of factors, the donor mutation, the immune system's response, the timing of antiretroviral therapy, drives the virus out of its hiding places. That knowledge could eventually inform approaches that don't require a matched donor or a bone marrow transplant.
For now, the Oslo patient remains off antiretroviral treatment with no detectable virus, five years after the transplant that treated his blood cancer and, apparently, his HIV as well.
