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Risky stem cell transplant cures 66-year-old man of leukemia, HIV

August 6, 2022

After undergoing a stem celltransplant to treat leukemia, a 66-year-old man may have been cured of HIV. Known as “The City of Hope Patient” after the City of Hope Cancer Centre where he was treated, he received a stem cell transplant for cancer treatment using cells from a donor with a rare genetic mutation, called CCR5-delta32, that blocks HIV from entering T-cells.

The patient, who wants to be anonymous, was diagnosed with HIV in 1988, his CD4 count declined so much that he was diagnosed with AIDS and started combination antiretroviral therapy when it became available in the mid-1990s.

In early 2019, at 63, he received a stem cell transplant from an unrelated donor with the CCR5-delta32 mutation to treat  acute myelogenous leukemia.

He received reduced-intensity chemotherapy and continued his antiretroviral therapy for two years after the transplant. With an undetectable viral load, he and his doctors decided to try a carefully monitored treatment interruption.

More than three years after the transplant, and over 17 months after stopping antiretrovirals, he has no evidence of HIV RNA rebound and no detectable HIV DNA. HIV antibody level has declined and his leukemia also remains in remission.

According to Dr Jana Dickter, of the City of Hope Cancer Centre, during the 24th  International AIDS Conference in Montreal, Canada, the patient has remained free of HIV for more than 17 months after stopping antiretroviral therapy.

He is the oldest person known to be cured of HIV after stem cell transplants. He has been living with HIV longer and it is expected that his treatment may open up the opportunity for older patients living with HIV and blood cancers to receive a stem cell transplant and go into remission for both diseases.

“We were thrilled to let him know that his HIV is in remission and he no longer needs to take antiretroviral therapy that he had been on for over 30 years,” Dickter said.

Although the transplant procedure is not likely to be an option for most people with HIV, the findings provide clues that could help researchers develop more widely applicable approaches for long-term HIV remission.

In the view of President-elect of the International AIDS Society, Dr Sharon Lewin, of the Peter Doherty Institute for Infection and Immunity in Melbourne: “These cases are still interesting, still inspiring and illuminate the search for a cure.”

Timothy Ray Brown was the first known to be cured of HIV after stem cell transplant. Known as the “Berlin Patient” Timothy received two transplants to treat leukemia in 2006.

His doctor, Gero Hütter, thought of the idea to use cells from a donor with the CCR5-delta32 mutation, speculating that it might cure both cancer and HIV.

Brown stopped antiretroviral treatment at the time of his first transplant, but his viral load did not rebound.

He was free of HIV for more than 13 years before he died in September 2020 from a recurrence of leukemia. Extensive testing of his blood, gut and other tissues showed no evidence of functional HIV anywhere in his body.

The second person to be cured was Adam Castillejo. Known as the “London Patient”, he had a stem cell transplant to treat lymphoma, receiving cells from a donor with the same mutation. He stopped ARV therapy 18 months after the transplant in September 2017 and has been HIV-free for more than four years.

A middle-aged woman with leukemia received a combination of umbilical cord blood cells with the CCR5-delta32 mutation and partially matched adult stem cells from a relative. She stopped antiretroviral therapy three years after the transplant, and her viral load remains undetectable a year and a half later.

Another individual, dubbed the “Dusseldorf Patient” has not experienced HIV rebound for more than three years after stopping antiretroviral therapy post-transplant.

Researchers are still trying to figure out why some people appear to be cured after stem cell transplants while other attempts have failed. Using stem cells from donors with the CCR5-delta-32 mutation appears to be a key to success.

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