Hidden HIV/AIDS Immunity
by Simon Zafrany and Nina Seale
The Student Newspaper
November 4, 2012
Throughout the course of history, diseases have shown their innate ability to bring human civilization to its knees. From the Bubonic Plague to Spanish Flu, these invisible menaces have indiscriminately struck down massive percentages of the human population; however, it seems as if our generation’s most notorious pandemic, HIV, may just be leaving a certain demographic of Europeans completely unscathed.
1.7 million people died of AIDS last year. Thought to have originated from non-human primates in sub-saharan Africa, since the first recorded human patients in 1959 it has become one of the most notorious diseases affecting the human population. But with almost every disease there are genes in the suffering population that fight back. And HIV is no different. One advantage of having such a huge population on Earth means the probability of resistance being hidden within the huge gene pool is high. And scientists have discovered that there is a gene floating around the European gene pool that could spell the end of the HIV pandemic: CCR5-Δ32.
The HIV virus works by hijacking certain cells associated with our immune system, which eventually destroys them and cripples the immune system of those infected (AIDS symptoms arise when the body is no longer able to properly defend itself from infections). This little mutation can prevent the HIV virus from entering these immune cells, by simply not producing the molecule that the virus uses as a trapdoor to enter human cells.
The trouble is that this mutation only exists within 20 per cent of ethnic western Europeans, and even then the individual needs two copies of this hidden mutation for complete, instead of partial, protection from HIV. However, the key to understanding this elusive gene, and hopefully harnessing its mechanisms for a cure, is the understanding of who has it and why. Gérard Lucotte, a French geneticist, set out to answer these questions. Lucotte and his team collected DNA samples from thousands of unrelated individuals from different European populations in order to map CCR5-Δ32 frequency. What his results revealed would shed light on the origins of this all-important allele as well as serve as an impetus for further research.
Within the tested populations, Lucotte found a considerable variation in frequency. Northern European populations showed estimated frequency levels of around 13 per cent and over 14 per cent in Scandinavian countries. In contrast, there was an increasing scarcity of CCR5-Δ32 the further south the research team ventured. Italians showed a mean frequency of 5.2 per cent, Portuguese 5.6 per cent, and Corsicans a staggeringly low 1.2 per cent. The pattern exhibited here clearly pointed to a genetic spread of the CCR5-Δ32 mutation from northern Europe, possibly Scandinavia, down to its southern neighbours.
Since looking into the origins of this mutation, researchers have been trying to work out how to harness it to find a cure for HIV. They have been trying to replicate the immunity mechanism by effectively locking the trapdoor molecules used by the HIV viruses to enter human cells with a specially designed drug.
Clinical trials of this treatment have been, so far, ineffective and there are other problems that have surfaced in individuals with this mutation (a higher frequency of a chronic liver disease), so CCR5-Δ32 based treatments for HIV might still be far away. But it may just be that the cure for this morbid virus has been waiting, written in our genes all along.
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