Who would have thought 10 years ago that there would be a cure for AIDS? Well, according to the Journal Watch: HIV/AIDS Clinical Care, February 13, 2009, a 40-year-old HIV positive male German patient with Leukemia underwent bone marrow stem cell transplantation, which completely eradicated the virus from his body, 2 years later. Removing HIV was not the main reason why the patient underwent the risky procedure, doctors at the Berlin Charité Hospital said.
The principal reason was to treat the patient for leukemia, a disease characterized by an uncontrollable increase or proliferation of malformed leukocytes and their precursors in the bone marrow and peripheral blood, caused by malignancy of the blood forming organs, National Institute of Health. Therefore, it was very unexpected to witnessed the complete absence of any HIV RNA traces, according to the doctors.
The process of transplanting healthy bone marrows into people with HIV, have been done many times before without any success of removing the virus from the body. So, one can understand why these doctors were not necessarily trying to use the procedure to cure the patient of AIDS, but instead, were trying to cure him of his leukemia problem.
Sometimes this is how a cure is achieved-by sheer accident. Well, mankind has one on its hands as we speak. One might be wondering what is so different about this bone marrow transplant and others done before it. The key ingredient is a defective version of the white blood cell protein chemokine receptor “CCR5.” This protein receptor and CXCR4 are both present on CD4 T-Cells and a few other immune system cells.
The HIV virus generally enters the white blood cell via the CCR5 receptor or the CXCR4 receptor. However, if the CCR5 or CXCR4 receptors are defective, the virus cannot access the T-Cells to infect them. HIV infections via the CXCR4 receptors are rare, but they do occur by variant strains of the virus, The Lancet, May 22nd 2002.
Our discussion will therefore focus on the CCR5 receptor. A very large percent of people have normal amounts of CCR5 receptors on their CD4 T-Cells. A few of us have limited or partial amounts while some of us have none at all. Well, in this instance, it pays to have none. People who have limited amounts of the CCR5 receptor are heterozygous for the gene that codes for it.
A gene is a small segment of a double helical DNA. The DNA itself contains two strands of nucleotides base pairs that are twisted in a spiral shape like a rope. The only difference is that there are only two strands within the DNA helix while there are several within the rope’s helix.
It is therefore a segment of this helix that is termed, the gene. It is just like cutting a small segment from a rope and examining the characteristics of that segment from the rope. In our case, we will be examining the piece of the DNA that codes for the CCR5 receptor, which is also a protein. We will find that in heterozygous individuals, only one section from one strand of the DNA codes for the defective CCR5 receptor, while the opposite section on the other strand of the DNA does not code for a defective version but codes for the normal CCR5 receptor, which facilitates easy HIV infection.
People who are homozygous in relationship to the defective genetic segment (32-bp deletion) on the DNA are therefore totally immune to the CCR5 mode of HIV infection. And if those people were ever going to get HIV, they will have to be infected with a HIV variant that strictly invades the CXCR4 receptor instead of the CCR5 receptor.
On the other hand, individuals who have normal proportions of CCR5 receptors on their CD4 T-Cells with no heterozygosity or homozygosity are 100% more susceptible to HIV infection. In fact, there are tests that can be done to determine whether or not a person is heterozygous or homozygous for the defective CCR5 gene.
The HIV positive patient who was cured by the stem cell transplant was given a stem cell that was taken from a person who was homozygous for the CCR5 deletion on his/her gene. Deletion means that the normal base pairings of the DNA segments (genes) was changed into something else that does not code for anything. It is not all segments on a DNA that codes for something useful. Therefore, this is why the CCR5 receptor does not work and is therefore defective.
Sometimes certain portions of the DNA are stop codes, blanks or codes that do not provide instructions to make any proteins. A perfect example of this is trying to build a car without a blueprint or a schematic. It does not matter how much material is available. If there is no instruction of how to build cars, there will be no cars built. Our example is the same way. The DNA and segments (gene) of the DNA are blueprints that cells use to build different proteins for the body.
The HIV positive patient in our discussion was obviously infected with the HIV strain that specifically uses the CCR5 receptor has its mode of entry into the CD4 T-cells. This patient will not be infected with HIV again unless he is exposed to an HIV variant that uses the CXCR4 mode of infection or something totally different. This scenario is very unlikely provided that the patient refrain from risky sexual behaviors.