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Public release date: 15-Mar-2012[ | E-mail |
Share ] Contact: Phyllis Edelman
pedelman@genetics-gsa.org
301-351-0896
Genetics Society of America
A new article in the journal Genetics suggests that even in early infection, when the virus population is low and has reduced genetic variation, HIV rapidly evolves to evade immune defenses and treatments
Bethesda, MD March 15, 2012 -- A new research report appearing in the March 2012 issue of the journal Genetics shows why the development of a cure and new treatments for HIV has been so difficult. In the report, an Australian scientist explains 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 Genetics. "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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ABOUT GENETICS: Since 1916, Genetics has covered high quality, original research on a range of topics bearing on inheritance, including population and evolutionary genetics, complex traits, developmental and behavioral genetics, cellular genetics, gene expression, genome integrity and transmission, and genome and systems biology. Genetics, the peer-reviewed, peer-edited journal of the Genetics Society of America is one of the world's most cited journals in genetics and heredity.
ABOUT GSA: Founded in 1931, the Genetics Society of America (GSA) is the professional membership organization for scientific researchers, educators, bioengineers, bioinformaticians and others interested in the field of genetics. Its nearly 5,000 members work to advance knowledge in the basic mechanisms of inheritance, from the molecular to the population level. The GSA is dedicated to promoting research in genetics and to facilitating communication among geneticists worldwide through its conferences, including the biennial conference on Model Organisms to Human Biology, an interdisciplinary meeting on current and cutting edge topics in genetics research, as well as annual and biennial meetings that focus on the genetics of particular organisms, including C. elegans, Drosophila, fungi, mice, yeast, and zebrafish. GSA publishes Genetics, a leading journal in the field and a new online, open-access publication, G3: Genes|Genomes|Genetics. For more information about GSA, please visit www.genetics-gsa.org. Also follow GSA on Facebook at facebook.com/GeneticsGSA and on Twitter @GeneticsGSA.
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AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
Public release date: 15-Mar-2012[ | E-mail |
Share ] Contact: Phyllis Edelman
pedelman@genetics-gsa.org
301-351-0896
Genetics Society of America
A new article in the journal Genetics suggests that even in early infection, when the virus population is low and has reduced genetic variation, HIV rapidly evolves to evade immune defenses and treatments
Bethesda, MD March 15, 2012 -- A new research report appearing in the March 2012 issue of the journal Genetics shows why the development of a cure and new treatments for HIV has been so difficult. In the report, an Australian scientist explains 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 Genetics. "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."
###
ABOUT GENETICS: Since 1916, Genetics has covered high quality, original research on a range of topics bearing on inheritance, including population and evolutionary genetics, complex traits, developmental and behavioral genetics, cellular genetics, gene expression, genome integrity and transmission, and genome and systems biology. Genetics, the peer-reviewed, peer-edited journal of the Genetics Society of America is one of the world's most cited journals in genetics and heredity.
ABOUT GSA: Founded in 1931, the Genetics Society of America (GSA) is the professional membership organization for scientific researchers, educators, bioengineers, bioinformaticians and others interested in the field of genetics. Its nearly 5,000 members work to advance knowledge in the basic mechanisms of inheritance, from the molecular to the population level. The GSA is dedicated to promoting research in genetics and to facilitating communication among geneticists worldwide through its conferences, including the biennial conference on Model Organisms to Human Biology, an interdisciplinary meeting on current and cutting edge topics in genetics research, as well as annual and biennial meetings that focus on the genetics of particular organisms, including C. elegans, Drosophila, fungi, mice, yeast, and zebrafish. GSA publishes Genetics, a leading journal in the field and a new online, open-access publication, G3: Genes|Genomes|Genetics. For more information about GSA, please visit www.genetics-gsa.org. Also follow GSA on Facebook at facebook.com/GeneticsGSA and on Twitter @GeneticsGSA.
[ | E-mail | Share ] ?
AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
Source: http://www.eurekalert.org/pub_releases/2012-03/gsoa-csh031412.php
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