The rapid evolution of HIV, which has allowed the virus to develop resistance to patients' immunity, is at the same time slowing the virus's ability to cause AIDS, according to a new research.
The study also suggested that people infected by HIV are likely to progress to AIDS more slowly because of widespread access to antiretroviral therapy (ART).
The study was led by researchers at the University of Oxford, along with scientists from South Africa, Canada, Tokyo, Harvard University and Microsoft Research.
The research was carried out in Botswana and South Africa, two countries that have been worst affected by the HIV epidemic. Across those countries, researchers enrolled over 2,000 women with chronic HIV infection to take part in the study.
The first part of the study looked at whether the interaction between the body's natural immune response and HIV leads to the virus becoming less virulent.
Central to this investigation are proteins in our blood called the human leukocyte antigens (HLA), which enable the immune system to differentiate between the human body's proteins and the proteins of pathogens.
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People with a gene that expresses a particular HLA protein called HLA-B*57, are known to benefit from a 'protective effect' to HIV. Infected patients with the HLA-B*57 gene progress more slowly than usual to AIDS.
The study showed that in Botswana, where HIV has evolved to adapt to HLA-B*57 more than in South Africa, patients no longer benefit from this gene's protective effect.
However, the team's data show that the cost of this adaptation to HIV is that its ability to replicate is significantly reduced, therefore making the virus less virulent.
The authors showed that viral adaptation to protective gene variants, such as HLA-B*57, is driving down the virulence of transmitted HIV and is thereby contributing to HIV elimination.
In the second part of the study the authors examined the impact of ART on HIV virulence. They developed a mathematical model, which concluded that selective treatment of people with low CD4 counts will accelerate the evolution of HIV variants with a weaker ability to replicate.
"This research highlights the fact that HIV adaptation to the most effective immune responses we can make against it comes at a significant cost to its ability to replicate," said lead scientist, Professor Phillip Goulder from the University of Oxford.