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Man appears free of HIV after stem cell transplant – FOR 3 YEARS!

Posted Feb 20 2009 12:00am


  • Doctors have not been able to detect the virus in his blood since about Jan of 2007.
  • In this case, there were 80 compatible blood donors living in Germany and on the 61st sample tested, they found one with the “retrovirus resistant” mutation from both parents.
  • There were no embryonic stem cells involved in this.  The stem cells in bone marrow are adult stem cells only.  Any time you see the words “treated” or “improved” or “recovered” associated with the words “stem cells”, assume it was from adult or repair stem cells until proven otherwise.

“A 42-year-old HIV patient with leukemia appears to have no detectable HIV in his blood and no symptoms after a stem cell transplant from a donor carrying a gene mutation that confers natural resistance to the virus that causes AIDS, according to a report published Wednesday in the New England Journal of Medicine.”


The startling case of an AIDS patient who underwent a bone marrow transplant to treat leukemia is stirring new hope that gene-therapy strategies on the far edges of AIDS research might someday cure the disease.

The patient, a 42-year-old American living in Berlin, is still recovering from his leukemia therapy, but he appears to have won his battle with AIDS. Doctors have not been able to detect the virus in his blood for more than 600 days, despite his having ceased all conventional AIDS medication. Normally when a patient stops taking AIDS drugs, the virus stampedes through the body within weeks, or days.

[Dr. Gero Hutter]
Sixten Koerper
Dr. Gero Hütter isn’t an AIDS specialist, but he ‘functionally cured’ a patient, who shows no sign of the disease.

“I was very surprised,” said the doctor, Gero Hütter.

The breakthrough appears to be that Dr. Hütter, a soft-spoken hematologist who isn’t an AIDS specialist, deliberately replaced the patient’s bone marrow cells with those from a donor who has a naturally occurring genetic mutation that renders his cells immune to almost all strains of HIV, the virus that causes AIDS.

Published December 14, 2010 – |

There’s an estimated 33 million people worldwide living with HIV/AIDS, and now doctors believe one of them may have been cured of the virus after receiving a stem cell transplant in 2007, the medical journal Blood reported.

Timothy Ray Brown, an HIV-positive American living in Germany, had leukemia and was undergoing chemotherapy, when he received a transplant of stem cells from a donor carrying a rare, inherited gene mutation that seems to make carriers virtually immune to HIV infection.

The transplant appeared to wipe out both diseases, giving hope to doctors, but Dr. Anthony Fauci, director of the National Institutes of Allergy and Infectious Diseases, who has been studying HIV/AIDS for almost 30 years, said while this is an interesting proof of concept, it’s absurdly impractical.

“It’s hard enough to get a good compatible match for a transplant like this,” Fauci told, “But you also have to find compatible donor that has this genetic defect, and this defect is only found in 1 percent of the Caucasian population and zero percent of the black population. This is very rare.”

Fauci said while this patient is “functionally cured” this is not something you can do with every HIV-infected individual.

“This is not prime time to me at all,” he said. “This is a very unusual situation that has little practical application for a simple reason. This donor not only had to be a good compatible match, but the donor had to have a genetic defect of cells that do not express the receptor that the HIV virus needs to enter the cell.”

Fauci also pointed to the fact that this transplant process is not only expensive, it’s incredibly painful and complicated, and requires the patient to start a whole new regimen of drugs.

“This patient is trading one poison for another. He may not have to be on antiretroviral drugs anymore, but he has to take immunosuppressant drugs now to prevent the rejection of his transplant cells. Again, what this is, is an interesting proof of concept, but it’s absolutely impractical.”

Dr. Thomas Quinn, director of Johns Hopkins Center for Global Health told that he is very familiar with the “Berlin patient” case.

“This was a new report that looked much deeper into whether HIV could still be present or lurking in the body in some way, not cured, and since the transplant he remains viral free and his cells appear to be resistant to infection,” he said.

Quinn said he agrees with the researchers on this case that it would be qualified as the first HIV cure, opening the door to alternative means of curing HIV.

“He [Brown] has been without therapy for three years and appears to be free of the virus,” he said. “It gives hope to the millions of people infected with HIV that cure is a feasible option in the future.”

Even though Brown’s procedure proved to be successful, Quinn also warns that this was a rare case and a bone marrow transplant is not a cure-all for other HIV patients.

“It is a near fatal procedure that he had to have done because of the leukemia, but this procedure is very expensive and you have to be transplanted with a donor who is shown to be already resistant to HIV,” Quinn said. “You’re asking for a tall order to replicate this in the future.”

Brown’s case was published in a February 2009 issue of the New England Journal of Medicine

Read more:


Volume 360:692-698  February 12, 2009  Number 7

Long-Term Control of HIV by CCR5 Delta32/Delta32 Stem-Cell


Gero Hütter, M.D., Daniel Nowak, M.D., Maximilian Mossner, B.S., Susanne Ganepola, M.D., Arne Müßig, M.D., Kristina Allers, Ph.D., Thomas Schneider, M.D., Ph.D., Jörg Hofmann, Ph.D., Claudia Kücherer, M.D., Olga Blau, M.D., Igor W. Blau, M.D., Wolf K. Hofmann, M.D., and Eckhard Thiel, M.D.


Infection with the human immunodeficiency virus type 1 (HIV-1) requires the presence of a CD4 receptor and a chemokine receptor, principally chemokine receptor 5 (CCR5). Homozygosity for a 32-bp deletion in the CCR5 allele provides resistance against HIV-1 acquisition. We transplanted stem cells from a donor who was homozygous for CCR5 delta32 in a patient with acute myeloid leukemia and HIV-1 infection. The patient remained without viral rebound 20 months after transplantation and discontinuation of antiretroviral therapy. This outcome demonstrates the critical role CCR5 plays in maintaining HIV-1 infection.
Source Information

From the Department of Hematology, Oncology, and Transfusion Medicine (G.H., D.N., M.M., S.G., A.M., O.B., I.W.B., W.K.H., E.T.) and the Department of Gastroenterology, Infectious Diseases, and Rheumatology (K.A., T.S.), Campus Benjamin Franklin; and the Institute of Medical Virology, Campus Mitte (J.H.) all at Charité Universitätsmedizin Berlin; and the Robert Koch Institute (C.K.) all in Berlin.

Drs. Hofmann and Thiel contributed equally to this article.

Full Text of this Article

This article has been cited by other articles:

  • Arababadi, M. K., Hassanshahi, G., Azin, H., Salehabad, V. A., Araste, M., Pourali, R., Nekhei, Z. (2010). No Association Between CCR5-{Delta}32 Mutation and Multiple Sclerosis in Patients of Southeastern Iran. Lab Med 41: 31-33 [Abstract] [Full Text]
  • Fauci, A. S., Folkers, G. K. (2009). Investing To Meet The Scientific Challenges Of HIV/AIDS. Health Aff (Millwood) 28: 1629-1641 [Abstract] [Full Text]
  • Bonsignori, M., Moody, M. A., Parks, R. J., Holl, T. M., Kelsoe, G., Hicks, C. B., Vandergrift, N., Tomaras, G. D., Haynes, B. F. (2009). HIV-1 Envelope Induces Memory B Cell Responses That Correlate with Plasma Antibody Levels after Envelope gp120 Protein Vaccination or HIV-1 Infection. J. Immunol. 183: 2708-2717 [Abstract] [Full Text]
  • Levy, J. A. (2009). The Unexpected Pleiotropic Activities of RANTES. J. Immunol. 182: 3945-3946 [Full Text]
  • (2009). All you need to read in the other general journals. BMJ 338: b627-b627 [Full Text]
  • (2009). Stem-Cell Transplantation Enables Long-Term HIV Control. AIDS Clin Care 2009: 1-1 [Full Text]
  • Levy, J. A. (2009). Not an HIV Cure, but Encouraging New Directions. NEJM 360: 724-725 [Full Text]


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