In the war against HIV, two major fronts are being tackled. First of all, reducing the number of new infections: a priority in order to lighten the burden of the pandemic. "But we should not forget the 39 million people living with HIV [at the end of 2022]. Seeking to cure them is just as important," said Yazdan Yazdanpanah, director of the French National Agency for AIDS Research (ANRS MIE), on Thursday, July 25, at the International AIDS Conference in Munich, Germany.

Here, the inventiveness of researchers knows no limits, reflected in the variety of their strategies to cure HIV. They all share the same objective: to dislodge the virus embedded in the cells of infected individuals. While antiretroviral treatments succeed in blocking HIV multiplication – preventing the virus' progression to AIDS and its attendant complications – they fail to eliminate the intruder, who takes refuge in "reservoir cells" scattered throughout the body. This complex reservoir comprises several types of immune cells: lymphocytes (notably found in lymph nodes), macrophages, "microglia" cells (nestled in the central nervous system), etc.

The virus persists by integrating its genetic material – or "provirus" – into their genome. This makes it undetectable to the immune system, but also inaccessible to antiretroviral drugs. Dormant, but ready to awaken as soon as patients interrupt their treatment. In fact, within six weeks, it becomes detectable again in the blood. "Very few reservoir cells are enough to trigger this viral rebound," points out Asier Saez-Cirion of Paris' Institut Pasteur.

But there are exceptions. Since 2008, researchers have had their eyes on very rare individuals – seven to date, six men and one woman – all considered "cured" of HIV infection. "Cured" or "in prolonged remission?" Experts are debating. Whatever the case, even though these people had stopped all antiretroviral treatment for years (up to more than 10 years), the virus remained undetectable in their blood or in biopsies. Their CD4 lymphocyte counts (the preferred targets of HIV) remained stable, indicating a prolonged absence of viral multiplication.

All seven had developed blood cancers, which required bone marrow transplants. In the first five cases, the marrow donor carried a mutation in a particular gene: the CCR5 gene governing the production of a protein (the CCR5 receptor) which, on the surface of human cells, is the entry point for the virus. When this gene carries the "Delta32" mutation (on both copies), the virus can no longer penetrate cells. This is how these very rare recoveries were explained.

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