An HIV-positive man went into remission after receiving bone marrow from his brother, which has a rare mutation that prevents the receptors to which HIV binds from working.
By Emma Gomez edited by Lewis asked.
Colorized transmission electron micrograph of numerous HIV-1 virus particles (blue) replicating from a segment of a chronically infected H9 T cell (red).
NIAID/Flickr (CC BY 2.0)
A 63-year-old man was functionally cured of HIV thanks to a bone marrow transplant. Although bone marrow donations have resulted in HIV remission in the past, this is the first time that a donation from a sibling of the recipient has occurred.
The man received a bone marrow donation from his brother, who carried a rare genetic mutation called RCC5Δ32 which confers resistance to HIV-1, the most common type of human immunodeficiency virus. When a person has two copies of this genetic mutation, the surface protein CCR5, which HIV typically binds to, cannot express itself on human immune cells called T cells. An article published today in Natural microbiology showed how, after the transplant, the donor cells had replaced the bone marrow cells of the HIV-positive man and that their genes contained two copies of one RCC5Δ32 mutation (not all cells in the recipient’s body have been replaced, however). His healthy T-cell count skyrocketed in the year after the procedure and remained at healthy levels after he stopped antiretroviral therapy (ART) – the standard treatment for HIV – two years later.
Antiretroviral drugs can stop HIV from reproducing in the body and spreading to other people. But they do not completely eliminate the virus: it remains in dormant reservoirs around the body. If an HIV-positive person stops taking ART, the virus starts to spread again.
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In the new study, researchers tested the recipient’s blood, intestinal tissue and bone marrow for reservoirs of HIV after bone marrow transplantation. They found no detectable HIV in places where it would normally persist in a person on ART.
“If this reaction does not occur in all or at least most immunological tissues, there could be a risk of rebound at some point,” says Marius Trøseid, an infectious disease specialist at Oslo University Hospital and co-author of the paper. “I think we have shown, for the first time, that this is a complete engraftment – both in the peripheral blood, which has been demonstrated in several other cases, in the bone marrow, which has also been demonstrated in a few other cases, and then also in the intestinal lining tissue, which we believe is essential for [a] heal.”
But this treatment is not yet available for most people living with HIV. Patients in New York City, London, Dusseldorf and other places that have achieved HIV remission after bone marrow transplantation from a donor with RCC5Each of the Δ32 mutations needed it for another reason, such as cancer treatment.
“This is really only for patients with other malignancies or medical problems requiring a transplant, because [by] by itself, it’s just too risky” compared to ongoing ART treatment, says Jingmei Hsu, an oncologist at NYU Langone Health’s Laura and Isaac Perlmutter Cancer Center and lead author of the study on a New York patient, who was not part of the new paper.
For recipients, bone marrow transplants pose significant risks, including serious infections, graft-versus-host disease (GVHD), in which donor cells attack the patient’s body, or even death. Thus, “the risk of transplantation must be significantly lower than the risk of the patient dying from their malignant tumor,” explains Trøseid.
Through various studies that have measured the effect of a bone marrow transplant on a person’s HIV status, scientists have seen the infection go into remission. even when the donor does not have two copies of the RCC5Δ32 mutation. Because the new study used donor cells from the patient’s sibling, it adds new information about how these transplants work.
If the cells are too different from those of the donor, transplant complications such as GVHD could be of greater concern, says Björn-Erik Ole Jensen, head of the infectious diseases department at the University Hospital Düsseldorf, who was not involved in this study. However, if the donor’s cells are too similar to those of the recipient, there is a risk that the treatment will fail to effectively destroy the infected T cells.
“[A sibling transplant] There may be a difference, but we don’t understand everything perfectly,” Jensen says. “That’s why all these cases are always interesting.”
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