Washington: A new study has shed light on why the researchers have failed to develop a cure and new treatments for HIV.
In the report, an Australian scientist explained how he used computer simulations to discover that a population starting from a single human immunodeficiency virus can evolve fast enough to escape immune defenses.
These results are novel because the discovery runs counter to the commonly held belief that evolution 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,” said Jack da Silva, Ph.D., author of the study from the School of Molecular and Biomedical Science at the University of Adelaide in Adelaide, Australia.
“Further insight into the precise genetic mechanisms by which the virus manages to so readily adapt to all the challenges we throw at it will, hopefully, lead to novel strategies for vaccines and other control measures.”
To make this discovery, da Silva used computer simulation to determine whether, under realistic conditions, the virus could evolve as rapidly as had been reported if the virus population started from a single individual virus.
This was done by constructing a model of the virus population and then simulating the killing of virus-infected cells by the immune system, along with mutation, recombination and random genetic changes, due to a small population size, affecting viral genes.
Results showed that for realistic rates of cell killing, mutation and recombination, and a realistic population size, that the virus could evolve very rapidly even if the initial population size is one.
“A cure for HIV/AIDS has been elusive, and this report sheds light on the reason,” said Mark Johnston, Ph.D., Editor-in-Chief of the journal.
“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,” Johnston added.
The study has been published in the journal Genetics.