One of the world’s most feared virus is
losing its edge. HIV is evolving to become less deadly and less
infectious, according to a major scientific study led by British
scientists.
The team at the University of Oxford has shown that it was taking longer for HIV infection to cause AIDS.
The rapid evolution of HIV, which has
allowed the virus to develop resistance to patients’ natural immunity is
at the same time slowing the virus’s ability to cause AIDS.
The study also indicates that people
infected by HIV are likely to progress to AIDS more slowly — in other
words the virus becomes less virulent — because of widespread access to
antiretroviral therapy (ART). Both processes make an important
contribution to the overall goal of the control and eradication of the
HIV epidemic.
Scientists said: “Twenty years ago the
time to AIDS was 10 years, but in the last 10 years in Botswana that
might have increased to 12.5 years. One might imagine as time extends
this could stretch further and further and in the future people being
asymptomatic for decades.”
In 2013, there were a total of 35 million people living with HIV worldwide according to the World Health Organization.
The study was led by researchers at the
University of Oxford, along with scientists from South Africa, Canada,
Tokyo, Harvard University and Microsoft Research.
Lead scientist Professor Phillip Goulder
from the University of Oxford, said: “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.
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.”
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 2000
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, which enable
the immune system to differentiate between the human body’s proteins and
the proteins of pathogens. People with a gene that expresses a
particular HLA protein called HLA-B57, are known to benefit from a
protective effect to HIV.
Infected patients with the HLA-B57 gene progress more slowly than usual to AIDS.
This study showed that in Botswana,
where HIV has evolved to adapt to HLA-B57 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 show that viral adaptation
to protective gene variants, such as HLA-B57, 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.
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