Press Release: New HIV Cure Research Released at the XIX International AIDS Conference

Thursday, 26 July, 2012 (Washington D.C, US) - A new study has been released at the XIX International AIDS Conference (AIDS 2012) in Washington today confirming that patients treated early and then taken off antiretroviral therapy have shown no signs of a resurgence of their HIV infection.

There exists a unique cohort of patients in France who became HIV infected, started therapy early, and were able to successfully stop therapy without having a resurgence of their HIV infection (the “Visconti Cohort”). The study confirms the benefits of treating HIV at the very early stages of infection.

"Six years after interruption of treatment, patients treated early on in the post-infection period present a perfect ability to control the HIV infection. The patients in the ANRS EP47 VISCONTI cohort possess an extremely low “reservoir” of HIV in the cells at a similar level to that of “HIV controller” patients.

“These results suggest that the antiretroviral treatment should be started very early after infection, said Charline Bacchus, lead researcher of the study at the French National Agency for Research on AIDS and Viral Hepatitis (ANRS):

There is an immensely valuable store of knowledge to be gained from analyzing the immunological characteristics that made therapy redundant for these patients and the VISCONTI group of patients is one of the key scientific reasons behind the renewed optimism in the search for an HIV Cure.

Another study was presented today at AIDS 2012 by Daniel Kuritzkes. They studied the persistence of HIV in two HIV-infected men who underwent allogeneic (foreign) stem cell transplantation for treatment of lymphoma. Both patients had been infected for many years, and had been on antiretroviral therapy that completely suppressed HIV replication, but continued to have detectable latent virus in their circulating lymphocytes prior to transplantation.

The patients received a milder form of chemotherapy (the “conditioning” regimen) prior to transplant, which allowed them to stay on their HIV medications throughout the transplant period. Although HIV was detectable in their cells immediately after transplant, over time the transplanted donor cells replaced the patients’ own lymphocytes.

As this occurred, the amount of HIV DNA detectable in the patients’ blood cells decreased and became undetectable. One patient has now been followed for nearly two years since his transplant and the other for three-and-a-half years. No traces of virus could be found in the patients’ plasma, nor were we able to recover virus from the patients’ CD4+ T-cells by a sensitive culture method. In addition, we observed a significant decline in HIV antibody levels (tests conducted by Dr. Michael Busch in San Francisco), providing additional evidence for a lack of ongoing exposure to HIV antigen.

In contrast to the “Berlin” patient, who received cells that were intrinsically resistant to HIV infection because they lacked a key HIV receptor (the CCR5 receptor), the cells our patients received were CCR5+. We believe that continuous administration of effective antiretroviral therapy protected the donor cells from becoming HIV infected as they eliminated and replaced the patients’ immune cells, effectively clearing the virus from the patients’ blood lymphocytes. Tissue sampling and analytic treatment interruption are needed to assess fully the extent of HIV-1 reservoir reduction following allogeneic stem cell transplantation.

Results from a study led by David Margolis at the University of North Carolina at Chapel Hill were also published this week in Nature. Margolis and his team showed that a dose of a drug that inhibits an enzyme involved in HIV silencing leads to rapid production of HIV RNA in the patient’s latently infected cells. This could make such previously unreachable viral reservoirs susceptible to curative strategies. For example, in combination with treatments that enhance host immune defense, unmasking latent virus might allow clearance of infection.

Results from a study led by David Margolis at the University of North Carolina at Chapel Hill were also published this week in Nature. Margolis and his team showed that a dose of a drug that inhibits an enzyme involved in HIV silencing leads to rapid production of HIV RNA in the patient’s latently infected cells. This could make such previously unreachable viral reservoirs susceptible to curative strategies. For example, in combination with treatments that enhance host immune defense, unmasking latent virus might allow clearance of infection.

Last week the Inaugural Global Scientific Strategy Towards an HIV Cure was launched amid renewed optimism from the world´s leading HIV/AIDS scientists that the future prospects for finding an HIV cure are increasing.

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