CCR5 Delta 32 - The HIV Gene

What is CCR5?

Some people have a genetic mutation that makes them resistant or partially immune to HIV. A 32-base pair deletion (delta 32) in the gene for the human chemokine receptor 5 (CCR5) is responsible for this. HIV needs to attach to the CCR5 receptor to infect CD4+ T cells. People with these mutations either have no CCR5 receptors or have far fewer CCR5 receptors than an average person. This greatly reduces the possibility of HIV infection.

Our test is a genetic test to see if you possess one (heterozygous) or two (homozygous) copies of this particular mutation. Studies indicate that two copies prevent infection by all but the rarest non-R5 strains, and one copy will provide some resistance to infection. A study in the Journal of Acquired Immune Deficiency Syndrome concludes that men who have sex with men who are heterozygous for the CCR5 Delta 32 mutation "had a 70% reduced risk of HIV infection" compared to those without the mutation.

A study in the May 22nd, 2002 publication of The Lancet indicates:

"The CCR5 delta 32 polymorphism confers a high degree of resistance against infection by HIV-1 strains that use the CCR5 receptor to enter host cells, the most transmitted strains from person to person. However, rare cases of HIV-1 infection in individuals homozygous for CCR5Δ32 have been reported. In all these instances, exclusive use of CXCR4 by virus isolates, or presence of V3 variable loop envelope sequences typical of CXCR4-using viruses, were reported. We did a case study of a man homozygous for the CCR5Δ32 deletion and infected with dual-tropic HIV-1, which caused rapid depletion of CD4 T cells."

The CCR5 delta 32 mutation we test for provides a benefit against most strains of HIV. Some rare strains of HIV infect via the CXCR4 receptor so by no means does a positive result for CCR5 delta 32 allow someone to engage in risky behavior. Still, it can provide relative peace of mind. Your test results indicate whether you are homozygous, heterozygous, or normal for the CCR5 delta 32 mutation.

The following video produced by pharmaceutical company Boehringer Ingelheim gives an overview of how HIV infects cells and shows the role of CCR5.


Why should I take this test?

If you are HIV negative, this test will indicate if you have fewer CCR5 receptors than the average person, making it less likely for you to become infected with HIV if you are exposed to it.

If you are HIV Positive, this test will indicate if you are likely to progress slower to AIDS than the average person

What do the results mean?

Our results indicate if you are homozygous, heterozygous, or wildtype for the CCR5 mutation. These mutations provide an indication of probable rates of infection and progression but we are only testing for a mutation. We do not tell if you are immune to HIV.

What do heterozygous and homozygous mean?

Everyone has two copies of every gene. Heterozygous means you have one copy of the normal gene and one copy of the gene with the mutation. Homozygous means both copies of the gene are the same; either both are normal or both contain the mutation.

How accurate is the test?

Our testing methods ensure greater than 99.99% accuracy. All samples are retested to eliminate the possibility of false positives and ensure the greatest possible accuracy.

How many people have the CCR5 Delta 32 gene?

The CCR5 Delta 32 gene is most prominent in individuals of European descent.

This is the percentage of CCR5 delta 32 in different ethnic populations:*
European Descent: 16%
African Americans: 2%
Ashkenazi Jew: 13%
Middle Eastern: 2-6%

*Fernando Arenzana-Seisdedos, Marc Parmentier b. Genetics of resistance to HIV infection: Role of co-receptors and co-receptor ligands. Semin Immunol. 2006 Dec;18(6):387-403
*Martinson. J, et al, Global Distribution of the CCR5 gene 32-basepair deletion Nat Genet. 1997 May;16(1):100-3
*Martinson, Jeremy J.; Hong, Lilya; Karanicolas, Rosea; Moore, John P. a; Kostrikis, Leondios G.a Global distribution of the CCR2-64I/CCR5-59653T HIV-1 disease-protective haplotype AIDS. 2000 March;14(5): 483-489