A 63-year-old man in Norway has been documented in long-term remission from HIV after receiving an allogeneic hematopoietic stem cell transplant (HSCT) from his brother. Reported in Nature Microbiology, the “Oslo patient” remained free of detectable HIV five years after HSCT, which was performed to treat myelodysplastic syndrome. Extensive testing of blood, gut tissue and bone marrow found no measurable viral reservoirs, marking the first reported case of HIV remission following a stem cell donation from a sibling.
Many previously reported HIV remissions after HSCT involved donors who carry the CCR5Δ32 mutation. CCR5 is a protein on immune cells that HIV commonly uses to enter and infect them; the CCR5Δ32 variant prevents expression of that receptor and blocks many strains of HIV. The Oslo patient’s donor brother was homozygous for CCR5Δ32, a trait believed to be central in achieving durable remission in several past cases. The mutation is uncommon overall but is found at higher frequencies in some European populations.
Researchers say this case adds to a small but growing set of transplant-associated remissions that are helping clarify how HSCT can eliminate HIV reservoirs. Experts have noted that each successful case yields insights into mechanisms of cure—for example, how the absence of CCR5, immune responses mounted by donor cells, and complications such as graft-versus-host disease (GVHD) may all interact. Clinicians caution, however, that multiple factors likely combine to produce remission rather than any single element alone.
HSCT is an intensive procedure: a patient’s own marrow and much of the immune system are ablated with chemotherapy or radiation, then replaced with donor stem cells that rebuild immunity. That process can sharply reduce the pool of cells that harbor latent, replication-competent HIV—the viral reservoirs that cause rebound when antiretroviral therapy (ART) is stopped. If the new immune system lacks CCR5, common HIV-1 strains may be unable to re-enter cells, increasing the chance that any remaining virus cannot reestablish infection.
Not all post-transplant remissions have relied on CCR5Δ32. Some patients have achieved durable remission after receiving grafts without the mutation, suggesting additional mechanisms such as a graft-versus-reservoir effect, where the incoming donor immune system recognizes and eliminates residual host cells that carry latent virus. GVHD itself and drugs used to prevent or treat it—agents like ruxolitinib and vedolizumab—may also influence the reservoir or the immune environment in ways that hinder HIV persistence.
Well-known previous cases include patients described in Berlin, London, and New York, and a Geneva case in which remission occurred without a CCR5Δ32-positive donor. Together, these rare outcomes are guiding research into what combinations of genetics, immune responses, transplant-related effects and adjunctive therapies can produce durable HIV remission.
Despite their scientific importance, HSCTs are not a practical cure for most people with HIV. The procedure carries substantial risk, including a sizable early mortality rate and the possibility of cancer relapse in transplant recipients. For that reason, HSCTs are generally pursued only when medically indicated for a separate life-threatening condition such as a hematologic malignancy.
By contrast, modern ART safely suppresses HIV to undetectable levels for most people, though it is not a cure and typically requires lifelong therapy. Even with viral suppression, some people living with HIV experience persistent immune activation and inflammation that can contribute to long-term health issues.
Researchers will continue studying these rare transplant remissions to tease apart the contributing factors and to translate lessons into safer, scalable approaches that could reduce treatment burden and improve long-term health outcomes for people living with HIV.