Why CCR5?

CCR5 is the primary focus of our group's papers. It is the coreceptor that primarily provides resistance against the M-tropic version of HIV-1. This genetic defect may prevent HIV-1 from infecting macrophages or slowing down the rate of infection and the rate of disease progression. In fact, a mutation deletion in both copies of the CCR5 gene has been found in certain individuals who have been multiply-exposed to the virus but have never become infected.

What is CCR5?

CCR5 is a chemokine receptor. These receptors are seven membrane-spanning molecules found on the surface primarily of cells in the immune system. When these receptor molecules bind their ligands, i.e. chemokines, the end result is to recruit cells of the immune system to the site of tissue damage or disease. HIV-1 takes advantage of the presence of these chemokine receptors to gain access to the cell via a fusion-mediated event.

What is a CCR5 "defect"?

A defect normally implies that the system has gone array, however, in some cases defects or simply modifications from the normal genetic code, are helpful. In this case the defective CCR-5 genes contain a 32-base pair (bp) deletion. This deletion causes a shift in the reading frame which results in a severely truncated protein which is unable to reach the cell surface. With this defect AIDS progression is slowed, allowing someone to survive longer. Thus, in this case the defect is actually protective.

Great, where can I get one?

Unfortunately, you can not simply inject a CCR5 defect. You must be born with it. Only a small percentage of us have the defect. It is estimated that  people of European descent are 81% wild-type, 18% heterozygote and 1% homozygote. Studies of populations from non-white regions such as Venezuela, Japan and Western and Central Africa have revealed no mutations in the CCR5 genes.

More References on CCR5 studies