CCR5-delta32

How it works

CCR5 is a protein on the surface of some immune cells. Most strains of HIV use it as a door. The virus attaches to CCR5 and pulls itself inside¹³. The delta32 variant is a deletion of 32 letters of DNA from the CCR5 gene. The shortened protein never reaches the cell surface¹. With no door, the virus cannot get in.

A person with two copies of delta32 has no working CCR5 and is resistant to nearly all common HIV strains. A person with one copy has fewer doors, and infection progresses more slowly¹. The protection is not total. Some rare HIV strains use a different protein, CXCR4, and can still infect¹. Beyond HIV, the variant seems mostly harmless, though carriers may be more vulnerable to West Nile virus¹.

How common it is

About 1% of people of Northern European descent have two copies, and 10% to 15% have one¹. The rate falls towards southern Europe and is close to zero in Africa, East Asia, and the Americas before European contact¹. HIV is too new to explain such a common variant. One hypothesis is that plague or smallpox in medieval Europe favoured carriers. Neither has been proven¹.

History and culture

In 2007, Timothy Ray Brown, an American living in Berlin, had both HIV and leukaemia. His doctor, Gero Hütter, chose a bone marrow donor with two copies of delta32². The transplant replaced his immune system with resistant cells. The virus never returned. His case was published in 2009 and he became known as the Berlin Patient, the first person cured of HIV². He died of leukaemia in 2020². A few more people have since been cured the same way, including Adam Castillejo, the London Patient⁴. The procedure is too dangerous to use for HIV alone.