Man remains HIV-free for six years after stem cell transplant

A Berlin patient has remained virus-free for more than six years after stopping HIV medication following a stem cell transplant.

The case adds to a small but growing number of apparent cures, and challenges the belief that donor cells must be inherently resistant to HIV.

Potential cures for HIV

Leading the team, Professor Christian Gaebler studies long-term HIV remission at Charité – Universitätsmedizin Berlin.

Across decades of research, only a small number of transplant recipients have ever reached durable HIV remission without drugs.

Earlier cures mostly relied on donors who lacked CCR5, a protein on immune cells that HIV uses to infect them.

In October 2015, doctors treated the Berlin patient’s leukemia with chemotherapy, followed by a stem cell transplant that replaced his damaged immune cells with donor-derived cells.

Because fully resistant donors were unavailable, clinicians used donor cells carrying one typical CCR5 gene and one mutation, a DNA change that can alter how the protein functions.

Donor cells that come from another person can also trigger immune attacks against remaining cells from the original patient.

When HIV treatment stopped

Five earlier cure cases used donors with a rare genetic trait that prevents most new immune cells from carrying CCR5.

The Berlin case also follows the Geneva case, where remission occurred without a CCR5-resistant donor, suggesting such resistance is not always required.

“The belief was that using HIV-resistant stem cells was essential,” said Professor Christian Gaebler.

During treatment, the Berlin patient stayed on antiretroviral therapy (ART), a drug combination that keeps HIV levels very low.

“The patient felt that he had waited long enough after the stem cell transplant,” said Professor Gaebler.

After the Berlin patient stopped ART, follow-up blood tests continued to show no HIV RNA in plasma, a key marker for remission.

Was the patient cured?

Researchers often wait years after stopping ART before calling a cure, because the dormant virus can rebound later.

In the Berlin patient, teams found no replication-competent virus, meaning no virus capable of forming new infectious particles, in blood or intestinal tissue.

The Berlin patient’s HIV-specific antibodies and T cell responses faded over time, which fits with no ongoing viral activity.

HIV persists because a viral reservoir – infected cells that stay quiet but carry HIV – can survive for years.

The virus can stitch HIV genes into human DNA, letting infected cells divide while the virus remains hard to spot.

ART blocks new infection cycles, yet this treatment usually cannot erase every infected cell that formed earlier.

What cleared the virus

One theory is that donor immunity removed remaining HIV-infected cells, a response linked to graft-versus-host disease, where donor immune cells attack tissues from the original patient.

The report also noted strong antibody-dependent cellular cytotoxicity in the Berlin patient near the time of transplantation, a process in which antibodies help killer cells destroy infected targets.

Successful transplants depend on tissue matching, where donor and recipient immune markers closely align, shaping how strongly donor cells attack the patient’s remaining cells.

The Berlin patient also carried one CCR5 delta 32 copy, which might alter where susceptible immune cells settle in the body.

Because donor-recipient genetics differ so much, most clinicians still treat transplant-related HIV cures as exceptions rather than a standard treatment plan.

Transplant risks remain

Even with better care, allogeneic transplants still carry serious risks and can be life-threatening for some patients.

That danger is why stem cell transplants are reserved for people who also need transplants for hard-to-treat cancers.

Patients can face severe complications, including infections and graft-versus-host disease, and many require long hospital stays and monitoring.

Treatment for HIV

UNAIDS put the number of people living with HIV in 2024 at 40.8 million. For most patients, daily ART keeps HIV suppressed, prevents illness, and supports a near-normal lifespan with care.

As of 2025, the WHO recommends injectable medicine called lenacapavir for PrEP, given twice-yearly for strong protection.

Some teams are testing gene editing to disable CCR5 in a patient’s own cells. This method must reach enough long-lived immune cells and avoid harmful off-target changes, which remains a major hurdle.

Other experiments use engineered T cells to hunt infected cells directly, aiming to shrink the reservoir without risky transplants.

What the Berlin case adds

The Berlin patient became the seventh person reported HIV-free after a transplant, and only the second without full CCR5 resistance.

“We thought you needed to transplant from donors that lack CCR5, it turns out that you don’t,” said Professor Ravindra Gupta.

If similar immune clearing occurs in other patients, this outcome could widen donor choices, although the approach remains rare.

Researchers now want more long follow-up and deeper tissue testing, because HIV can hide outside the blood.

The goal is to copy the useful immune effects without the dangerous transplant, so more people could benefit.

The study is published in the journal Nature.

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