2024-07-30 04:00:21
In the war against HIV, two main fronts are open. Reducing the number of new infections, first: a priority, to ease the epidemic burden. “But we must not forget the 39 million people who have HIV [fin 2022]. Seeking to heal them is just as important”underlined Yazdan Yazdanpanah, director of the National AIDS Research Agency (ANRS-MIE), Thursday July 25, during the International AIDS Conference (AIDS), in Munich (Germany).
Here, the inventiveness of researchers is unlimited. This is evidenced by many of their HIV recovery strategies. With the same goal: to release the virus that is in the cells of infected individuals. Because if antiretroviral treatments are successful in preventing the multiplication of HIV – thus progressing to the stage of AIDS and its complications – they fail to eliminate the virus, which takes protection in the “reservoir cells” scattered throughout the body. A dense reservoir, containing many types of immune cells: lymphocytes (mainly found in lymph nodes), macrophages, “microglia” cells (egg cells in the central nervous system), etc. go.
The virus proceeds by integrating its genetic material – or “provirus” – into their genome. And we are not found for the immune system, but can not access antiretrovirals. Close, but ready to wake up once patients stop treatment. In the next six weeks, in fact, it became available in the blood again. “Very few reservoir cells are enough to cause this virus to replicate”underlines Asier Saez-Cirion, of the Institut Pasteur, in Paris.
Seven people are considered “supervisors”
But there are exceptions. Since 2008, researchers have set their sights on extremely rare individuals – seven to date, six men and one woman – all considered “the cure” of HIV infection. “Caught” or “in late remission”? Experts argue it. In any case, even though these people have stopped all antiretroviral treatment for years (more than a decade), the virus cannot be detected in their blood or in biopsies. Their level of CD4 lymphocytes (targets of HIV), for its part, remains stable, a sign of a long absence of virus multiplication.
These seven people all had leukemia, the treatment of which required a bone marrow transplant. In the first five, the fat donor carries a mutation in a specific gene: the CCR5 gene, which controls the production of a protein (CCR5 receptor) which, on the surface of human cells, is the gateway to the entry of the virus. When this gene carries the “Delta32” mutation (on both copies), the virus can no longer enter cells. This is how we explain very rare cures.
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