Dr Jack da Silva from the University’s School of Molecular & Biomedical Science has used computer simulations to discover that even in early infection when the virus population is low, HIV rapidly evolves to evade immune defences and treatments.
These results – published in this month’s issue of the prestigious journal GENETICS – challenge the commonly held belief that evolution of the virus under these circumstances is very slow.
“I believe the search for a cure for AIDS has failed so far because we do not fully understand how HIV evolves,” Dr da Silva said.
To make this discovery, Dr da Silva used computer simulations to determine whether, under realistic conditions, the virus could evolve rapidly if an infection started from a single virus.
This was done by constructing a model of the virus population, then simulating the killing of virus-infected cells by the immune system, along with mutation, recombination (the process by which genetic material is broken and joined to other genetic material), and random genetic changes.
Results show that for realistic rates of cell killing, mutation and recombination, and a realistic population size, the virus could evolve very rapidly even if the initial population size is one.
“At low population levels, viruses have reduced genetic variation and therefore it should be harder for them to evolve rapidly. However, it appears that the evolution of HIV goes against conventional wisdom,” Dr da Silva said.
“We now need further insight into the precise genetic mechanisms that enable the virus to so readily adapt to all the challenges we throw at it. Such knowledge will, hopefully, lead to novel strategies for vaccines and other control measures.”
Mark Johnston, Editor-in-Chief of GENETICS, said: “Now that we know HIV rapidly evolves, even when its population size is small, we may be able to interfere with its ability to evolve so we can get the most out of the treatments that are developed.”
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The full report from Dr Jack da Silva can be read online.