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Transplant success reignites interest in reprogramming cells against HIV

Editing cells to lack the CCR5 receptor may prove more feasible for more people.
  1. Colin Barras
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T cells infected with HIV. Comstock/Stockbyte/Getty

Last week, researchers took a small but significant step forward in the battle against HIV. A person named in public only as the ‘London patient’ has apparently been left free of the virus after a bone marrow transplant for a form of blood cancer. The announcement — made jointly at the Conference on Retroviruses and Opportunistic Infections in Seattle, Washington, and in a Nature paper1 — came with the caveat that the procedure is too risky and expensive to adopt widely for treatment of HIV. However, it has also sparked new interest in a technique to combat the virus by reprogramming the human immune system using gene-editing technology. HIV wreaks havoc on the immune system by forcing its way inside CD4 T immune cells, within which the virus replicates itself and ultimately destroys the cells. However, since the mid-1990s, researchers have been aware of a vulnerability in this attack strategy. HIV typically enters T cells by targeting a protein called C-–C chemokine receptor type 5 (CCR5), found on the cell surface. By chance, about 1–3% of people of European descent produce only non-functioning forms of CCR52. This altered version makes it much harder for HIV to enter their T cells3, breaking the viral replication cycle.

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doi: https://doi.org/10.1038/d41591-019-00011-y

**An earlier version of this story included a quote that mischaracterized the status of a clinical study. The article had stated: There were concerns that CSL Behring was keen to drop Calimmune’s HIV work, even though the clinical trial was at an advanced stage. Those fears proved well-founded. “Calimmune has been acquired and is no longer pursuing this study, which has been terminated,” says Ronald Mitsuyasu, a professor of medicine in hematology–oncology at the University of California, Los Angeles, who was the principal investigator on the clinical trial. The phase 1/2 study was actually completed. The agent did not move into a phase 3 trial; however, CSL Behring is funding an additional external study that might be able to demonstrate efficacy. The story has been updated for accuracy.

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