CCR5-Δ32 — HIV resistance variant
One copy of the CCR5-Δ32 deletion detected.
You have one copy of the CCR5-Δ32 deletion, a well-known DNA change linked to HIV resistance.
One-copy carriers have somewhat slowed HIV disease progression if infected, but are not protected from acquiring HIV.
If you have one copy, you can still catch HIV, but the disease tends to progress more slowly once it takes hold.
What this means
CCR5 is the co-receptor most strains of HIV use to enter immune cells. The Δ32 deletion produces a non-functional receptor. Homozygotes are largely protected from HIV-1 infection by R5-tropic strains — this is the mechanism behind the famous "Berlin patient" who was functionally cured by a stem-cell transplant from a CCR5-Δ32 donor. Heterozygotes have slower disease progression if infected but no infection protection.
CCR5 is a doorway on the surface of your immune cells that most HIV strains use to break in. The Δ32 deletion is a small chunk of missing DNA that means the doorway never forms properly. If you have two copies of the deletion, the doorway is essentially shut and you're strongly protected against the most common form of HIV — this is the mechanism behind the famous "Berlin patient," who was functionally cured of HIV after a stem-cell transplant from a donor with two copies. With one copy, you can still get HIV but it tends to progress more slowly.
Caveats
- Resistance is to R5-tropic HIV-1. Other HIV strains (X4-tropic) are not affected.
- There is some evidence of slightly worse West Nile virus outcomes; the trade-off is small.
- This is an informational finding for most people, not a basis for changing behaviour.
Populations
- Most common in Northern European populations (~10% allele frequency); rare elsewhere