Healthcare experts have always been puzzled at the fact that a small minority of those people who get infected with the HIV virus do not develop the full disease, AIDS. Investigators have been looking at what mechanisms underlie this resistance, in hopes of replicating them in the lab, and then turning them into drugs for those who already have the unforgiving disease. Scientists working in HIV research have thus far failed to come up with a satisfactory explanation for the phenomenon, but now a group of experts belies it may have found the answer,
Nature News reports.
The study was conducted by researchers at the Massachusetts Institute of Technology (MIT) in Cambridge, who were led by immunology expert Arup Chakraborty. Early results of the investigation, which also included specialists from New York and California, show that the varied response to HIV could be triggered by significant differences in the way immune system cells known as T cells develop inside those who do not get AIDS. The finding could bring the goal of creating a new HIV vaccine a lot closer to reality, given that experts now know early education of these T cells is key to getting them to stave off the action of HIV.
They way T cells work is being activated by human leukocyte antigens (HLA). These are cell-surface proteins that collect viral fragments and bacteria, and then present them to the immune cells. But first, the T cells need to be produced in a gland called the thymus. They basically go to school there, learning to recognize various pathogens, and also how not to overreact when they identify an infection. They are allowed out of the thymus only when they have already proven their worth. In the new study, the science team discovered that elite controllers – those people resistant to AIDS – exhibit a particular form of HLA, which is called HLA B57. This finding is tightly related to the fact that people who do not get AIDS even though they have the virus tend to develop autoimmune diseases.
In these conditions, cells of the immune system begin attacking other cells and organs in the human body, causing it to shut down from the inside. The correlation between the two observations is detailed in the May 5 online issue of the esteemed scientific publication Nature. Chakraborty found that HLA B57 and HLA B27 tend to bind to a much smaller proportion of self-peptides, which are substances on which T cells “train” while in the thymus. Non-protective HLA bind to a much wider variety of these molecules, the team reports.