CCR5 AS IMMUNITY OF AIDS

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. 

                                                                                                                                                        "CCR5-delta32" is a deletion mutation of a gene which only 1% of the total population has two copies of this gene and individuals who carry two copies of this genetic mutation are immune to Smallpox, The Bubonic Plague (Black Death) and HIV, the virus that causes AIDS. Up to 20% of the population carry only one copy of this genetic mutation depending on your background and although they still run a significant risk of contracting HIV, the progress of the disease is greatly reduced and can result in a longer life expectancy.

 
Cysteine-cysteine chemokine receptor 5 (CCR5) is found in the cell membranes of  many types of mammalian cells, including nerve cells and white blood cells. The role of CCR5 is to allow entry of chemokines into the cell—chemokines are involved in signaling the body’s inflammation response to injuries. The gene that codes for CCR5 is situated on human chromosome 3. Various mutations of the CCR5 gene are known that result in damage to the expressed receptor. One of the mutant forms of the gene is CCR5-delta32, which results from deletion of a particular sequence of 32 base-pairs. This mutant form of the gene results in a receptor so damaged that it no longer functions. But surprisingly, this does not appear to be harmful.
  This mutation can be advantageous to those individuals who carry it. The virus HIV normally enters a cell via its CCR5 receptors, especially in the initial stage of a person becoming infected. But in people with receptors crippled by the CCR5-delta32 mutation, entry of HIV by this means is blocked, providing immunity to AIDS for people with delta 32 mutation on both genes (called homozygous carriers) and greatly slowing progress of the disease in people with a delta 32 mutation on one of the two genes (called heterozygous carriers).
 
The importance of the protein CCR5 in HIV/AIDS treatment research. CCR5 is a protein on the surface of immune cells. Some people have a genetic mutation, called Delta-32, which alters how that protein works, how often it appears, or changes its structure. People with the mutation have immunity to some strains of HIV, the virus that causes AIDS.CCR5 is the key to the Berlin Patient—Timothy Ray Brown—who, until recently, was the only person to ever be cured of AIDS. Brown received bone marrow transplants from people who had the Delta-32 mutation. His body has been HIV-free for five years. And, last week, researchers announced that two other people successfully received the same treatment.But here's the thing, until today, I didn't totally understand how the connection between CCR5, Delta-32, and HIV worked. There's a story (and some great digital illustrations) on NPR's Shots blog that makes the situation much more clear. HIV, apparently, have little spikes all over its surface. These spikes are how the virus injects itself into cells.

Don't play with AIDS, it kills.