A collaborative study by European, Australian and American researchers has revealed some of the genetic mysteries as to why some people naturally keep HIV levels almost undetectable, whereas others quickly lose control of the infection.

The international collaboration is by far the largest to study the genetic differences between patients infected by HIV and is also the first study of this kind in the field of infectious disease.

In the study, published in Science, research was conducted with the latest genomics and bioinformatics technologies, analysing 550,000 variations of the complete human genome in 486 patients, mostly European, pre-selected from 30,000 potential candidates.

These variations, known as simple nucleotide polymorphisms (SNPs), are single variations affecting only one nucleotide or base of the genomic sequence. Despite humans sharing 99.9% of the genome sequence, there are still 3 million genetic variations – which make individuals different from one another – 90% of which are due to SNPs. Hence a good knowledge of these variations is highly valuable for the determination of the progression of AIDS.

The genetic data obtained was compared to blood virus load in patients during the first two years after the infection, and also to the rhythm of immune degradation as a result of the infection. This type of comparison, known as association study, permitted deduction of main genetic variations playing a central role in the control of viral infection.

The results point to two gene variants related to the immune system. More specifically, these variations are in a genetic region responsible for the determination of immune response capacity against a number of infectious diseases, including AIDS.

These variations are located in the short arm of chromosome 6 in genes controlling HLA-B and HLA-C molecular systems, responsible for the activation of the immune system so that it is able to locate and destroys cells infected by HIV.

The study also identified a third genetic variation involved in immunity damage of patients, particularly in a gene encoding a protein which seemingly participates in viral replication, and is also located in chromosome 6.

Genetic variants associated to genes encoding HLA-B and HLA-C molecular systems would explain up to 15% of viral load variation among patients, whereas the third genetic variation would explain 5.8% of these differences.

Though further study of other genetic regions involved in this process is needed, HLA-B variation presents the highest correlation with the immune response described until now.

Researchers claim that the information obtained would be very useful in the long road to the development of a more rational vaccine. The study would also lead to developing more personalised medicine, where the most suitable drugs for each individual would be determined on the basis of his or her gene characteristics.

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