It's possible that HIV's ability to cause AIDS is slowing. A new paper from Oxford University suggests the disease is becoming less deadly and less infectious over time as it adapts to our immune system and therapies.

The new study, which appears in the Proceedings of the National Academy of Sciences, shows that HIV's virulence may be declining due to increasing access to antiretroviral therapies (ARTs) and the ever-growing number of mutations that allow HIV to escape even the most effective immune responses generated against it.

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Consequently, people infected by HIV are now likely to progress to AIDS more slowly. The researchers say this quick evolution, which allows it to resist a person's natural immunity, is at the same time slowing the virus's ability to cause AIDS. So rather than making HIV stronger, our therapies are making it weaker.

"Overall we are bringing down the ability of HIV to cause AIDS so quickly," noted lead researcher Philip Goulder in a Reuters article. "But it would be overstating it to say HIV has lost its potency — it's still a virus you wouldn't want to have."

It's welcome news for researchers as they work to control the HIV epidemic which currently affects 35 million people worldwide. The disease has killed 40 million people since it began spreading 30 years ago.

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According to the researchers, the annual number of new HIV infections is lower than the number of HIV positive people being added to those receiving treatment. It suggests that a crucial tipping point has been reached in reducing deaths from AIDS.

The findings were made as part of an investigation to determine whether the interaction between the body's natural immune response and HIV leads to the virus becoming less virulent. The researchers enrolled over 2,000 women with chronic HIV infection from Botswana and South Africa. A press release from Oxford University explains the researchers' findings:

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. People with a gene for a particular HLA protein called HLA-B*57, are known to benefit from a 'protective effect' to HIV. That is, infected patients with the HLA-B*57 gene tend to progress more slowly than usual to AIDS.

This 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 the virus' ability to replicate is significantly reduced – making the virus less virulent.

The researchers show 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.

The researchers also developed a mathematical model to study the impact of ARTs on HIV virulence. It appears that the way treatment is provided to those with the more deadly form of HIV is hastening the evolution of HIV viruses by endowing it 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," noted Goulder. "Anything we can do to increase the pressure on HIV in this way may allow scientists to reduce the destructive power of HIV over time."

To which the Wellcome Trust's Mike Turner added: "The widespread use of ART is an important step towards the control of HIV. This research is a good example of how further research into HIV and drug resistance can help scientists to eliminate HIV."

Read the entire study at PNAS: "Impact of HLA-driven HIV adaptation on virulence in populations of high HIV seroprevalence".

Image: martynowi.cz/Shutterstock

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