CCR5-delta32: The Gene Deletion That Makes Some People Resistant to HIV
One deleted stretch of DNA can slam shut the door HIV uses to infect cells — the science behind the world's only cured patients.
A small deletion in a single gene — CCR5-delta32 — makes some people naturally resistant to the most common form of HIV. It's one of the most remarkable stories in human genetics: the basis of the only people ever confirmed cured of HIV, and a cautionary tale about the ethics of gene editing.
How HIV gets into cells — and how this gene blocks it
To infect an immune cell, HIV has to dock onto proteins on the cell's surface. The main receptor is CD4, but HIV also needs a "co-receptor" — usually a protein called CCR5 — to actually get inside. Think of CCR5 as a second lock the virus must pick to enter.
The CCR5 gene codes for that co-receptor. A variant called delta32 is a 32-base-pair deletion that garbles the gene, so the CCR5 protein isn't properly made or displayed on the cell surface. No functional CCR5 on the surface means the most common (CCR5-tropic) strains of HIV can't get in — the lock is missing.
One copy vs. two
Zygosity matters a great deal here:
- Two copies (homozygous delta32) — strong resistance to CCR5-tropic HIV, because virtually no functional co-receptor is made.
- One copy (heterozygous) — not fully resistant, but associated with slower disease progression in some people, since there's less CCR5 available.
The variant is most common in people of Northern European ancestry and rarer elsewhere — an intriguing distribution that researchers have long tried to explain, with various historical hypotheses about what selective pressure might have favored it.
The "Berlin Patient" and the world's only HIV cures
This gene isn't just a curiosity — it's behind the only confirmed HIV cures. The famous "Berlin Patient" (and a small number of patients since) was cured of HIV after receiving a bone-marrow transplant, for cancer, from a donor who happened to be homozygous for CCR5-delta32. The transplanted immune system, lacking functional CCR5, was resistant to the virus — and the patient's HIV became undetectable off medication. It's a stunning proof of concept, though the procedure itself is far too risky and drastic to be a general treatment.
The gene-editing cautionary tale
CCR5 is also central to one of the most controversial episodes in modern science. A researcher attempted to edit CCR5 in human embryos to try to confer HIV resistance, resulting in the birth of gene-edited babies. The experiment was widely condemned by the scientific community as premature, unethical, and dangerous — the health effects were unknown, consent was impossible, and the risks were unjustifiable. It became a defining example of why heritable human gene editing is subject to such serious ethical and safety scrutiny.
Curious Whether You Carry CCR5-delta32?
A whole genome sequence reads your CCR5 status directly — one of the most scientifically famous variants in the human genome — alongside thousands of other well-studied markers. It's part of the fascinating story your own DNA can tell.
Get 10% Off Whole Genome Sequencing → Use code GENOME at checkout · Italian lab · Full 30x WGS · You keep the raw dataAn important reality check
Even people homozygous for delta32 are not invincible against HIV: some HIV strains use a different co-receptor (CXCR4) and can bypass the missing CCR5 lock entirely. So this variant confers strong resistance to the common CCR5-tropic strains, not blanket immunity. Nothing about carrying delta32 changes the importance of standard prevention. The value here is scientific insight into your own genome — not a license to take risks.
This article is for general educational purposes only and is not medical advice. Genetic results should be interpreted with a qualified healthcare provider or genetic counselor. Do not start, stop, or change any medication or treatment based on this article.