Sally Furniss
Well-known member
Abstract
Annual Review of Ecology, Evolution, and Systematics
Vol. 38: 27-52 (Volume publication date December 2007)
(doi:10.1146/annurev.ecolsys.38.091206.095637)
<!-- End title of page and review --><!-- Start full text content --> First published online as a Review in Advance on June 28, 2007
<!-- abstract content -->Virus Evolution: Insights from an Experimental Approach
<nobr>Santiago F. Elena and </nobr>*<wbr><nobr>Rafael Sanju?n</nobr>*<wbr>Instituto de Biolog?a Molecular y Celular de Plantas, Consejo Superior de Investigaciones Cient?ficas-Universidad Polit?cnica de Valencia, 46022 Val?ncia, Spain; email: sfelena@ibmcp.upv.es
Abstract Viruses represent a serious problem faced by human and veterinary medicine and agronomy. New viruses are constantly emerging while old ones evolve and challenge the latest advances in antiviral pharmaceutics, thus generating tremendous social alarm, sanitary problems, and economical losses. However, they constitute very powerful tools for experimental evolution. These two faces of virology are tightly related because future antiviral treatments shall be rationally designed by considering evolutionary principles. Evidence indicates that the evolution of viruses is determined mainly by key features such as their small genomes, enormous population sizes, and short generation times, and at least for RNA viruses, large selection coefficients, antagonistic epistasis, and high mutation rates. We summarize recent advances in the field of experimental virus evolution. Increasing our understanding of the roles of selection, mutation, chance, and historical contingency on the ecology and epidemiology of viral infections could determine our ability to combat them.
Acronyms and Definitions
Antagonistic epistasis: when the combined effect of mutations is weaker than expected from their individual effects
Arboviruses: viruses that use arthropods as vectors of transmission
Complementation: interaction between two viral genomes within an infected cell such that the virus can function despite each genome carrying different mutated, nonfunctional genes
Effective population size (N<sub>e</sub>): the number of viral particles that effectively contribute to the next infectious cycle
Error threshold: critical mutation rate beyond which selection cannot further maintain the information encoded in the genome
Fitness: the number of descendants an individual generates per time unit, usually relative to that of a reference genotype
FMDV: foot-and-mouth disease virus
Genetic drift: changes in genotypic frequencies due to random sampling between generations
Genomic deleterious mutation rate (U<sub>d</sub>): the number of deleterious mutations produced per genome and replication round
HIV-1: human immunodeficiency virus type 1
L: mutational load
Lethal mutagenesis: the deterministic extinction of a population due to an excessive mutation rate
MOI: multiplicity of infection
Mutational robustness: the constancy of phenotypic expression in the face of mutation
RdRp: RNA-dependent RNA polymerase
RT: reverse transcriptase
Selection coefficient (s): the relative fitness difference between a mutant genotype and the wild type
Synergistic epistasis: when the combined effect of mutations is stronger than expected from their individual effects
VSV: vesicular stomatitis virus
<!-- /abstract content --><!-- fulltext content --><table align="center"><tbody><tr><td align="center" nowrap="nowrap" width="80">Full Text</td><td align="center" width="50">PDF
http://arjournals.annualreviews.org/doi/abs/10.1146/annurev.ecolsys.38.091206.095637
</td></tr></tbody></table>
Annual Review of Ecology, Evolution, and Systematics
Vol. 38: 27-52 (Volume publication date December 2007)
(doi:10.1146/annurev.ecolsys.38.091206.095637)
<!-- End title of page and review --><!-- Start full text content --> First published online as a Review in Advance on June 28, 2007
<!-- abstract content -->Virus Evolution: Insights from an Experimental Approach
<nobr>Santiago F. Elena and </nobr>*<wbr><nobr>Rafael Sanju?n</nobr>*<wbr>Instituto de Biolog?a Molecular y Celular de Plantas, Consejo Superior de Investigaciones Cient?ficas-Universidad Polit?cnica de Valencia, 46022 Val?ncia, Spain; email: sfelena@ibmcp.upv.es
Abstract Viruses represent a serious problem faced by human and veterinary medicine and agronomy. New viruses are constantly emerging while old ones evolve and challenge the latest advances in antiviral pharmaceutics, thus generating tremendous social alarm, sanitary problems, and economical losses. However, they constitute very powerful tools for experimental evolution. These two faces of virology are tightly related because future antiviral treatments shall be rationally designed by considering evolutionary principles. Evidence indicates that the evolution of viruses is determined mainly by key features such as their small genomes, enormous population sizes, and short generation times, and at least for RNA viruses, large selection coefficients, antagonistic epistasis, and high mutation rates. We summarize recent advances in the field of experimental virus evolution. Increasing our understanding of the roles of selection, mutation, chance, and historical contingency on the ecology and epidemiology of viral infections could determine our ability to combat them.
Acronyms and Definitions
Antagonistic epistasis: when the combined effect of mutations is weaker than expected from their individual effects
Arboviruses: viruses that use arthropods as vectors of transmission
Complementation: interaction between two viral genomes within an infected cell such that the virus can function despite each genome carrying different mutated, nonfunctional genes
Effective population size (N<sub>e</sub>): the number of viral particles that effectively contribute to the next infectious cycle
Error threshold: critical mutation rate beyond which selection cannot further maintain the information encoded in the genome
Fitness: the number of descendants an individual generates per time unit, usually relative to that of a reference genotype
FMDV: foot-and-mouth disease virus
Genetic drift: changes in genotypic frequencies due to random sampling between generations
Genomic deleterious mutation rate (U<sub>d</sub>): the number of deleterious mutations produced per genome and replication round
HIV-1: human immunodeficiency virus type 1
L: mutational load
Lethal mutagenesis: the deterministic extinction of a population due to an excessive mutation rate
MOI: multiplicity of infection
Mutational robustness: the constancy of phenotypic expression in the face of mutation
RdRp: RNA-dependent RNA polymerase
RT: reverse transcriptase
Selection coefficient (s): the relative fitness difference between a mutant genotype and the wild type
Synergistic epistasis: when the combined effect of mutations is stronger than expected from their individual effects
VSV: vesicular stomatitis virus
<!-- /abstract content --><!-- fulltext content --><table align="center"><tbody><tr><td align="center" nowrap="nowrap" width="80">Full Text</td><td align="center" width="50">PDF
http://arjournals.annualreviews.org/doi/abs/10.1146/annurev.ecolsys.38.091206.095637
</td></tr></tbody></table>