Some articles of interest, with quotes from abstracts, from the Theme Issue ‘New experimental and theoretical approaches towards the understanding of the emergence of viral infections’ compiled and edited by Santiago F. Elena and Rémy Froissart – Philosophical Transactions of the Royal Society BJune 27, 2010 365 (1548):
98% identical, 100% wrong: per cent nucleotide identity can lead plant virus epidemiology astray (by Duffy, S., Seah, Y. M.)
(…) Many of these sentinel publications include viral sequence data, but most use that information only to confirm the virus’ species. When researchers use the standard technique of per cent nucleotide identity to determine that the new sequence is closely related to another sequence, potentially erroneous conclusions can be drawn from the results. Multiple introductions of the same pathogen into a country are being ignored because researchers know fast-evolving plant viruses can accumulate substantial sequence divergence over time, even from a single introduction. (…)
The virulence-transmission trade-off in vector-borne plant viruses: a review of (non-)existing studies (by Froissart, R., Doumayrou, J., Vuillaume, F., Alizon, S., Michalakis, Y.)
The adaptive hypothesis invoked to explain why parasites harm their hosts is known as the trade-off hypothesis, which states that increased parasite transmission comes at the cost of shorter infection duration. (…) We found only very few appropriate studies testing such a correlation, themselves limited by the fact that they use symptoms as a proxy for virulence and are based on very few viral genotypes. Overall, the available evidence does not allow us to confirm or refute the existence of a transmission–virulence trade-off for vector-borne plant viruses. (…)
Pathways to extinction: beyond the error threshold (by Manrubia, S. C., Domingo, E., Lazaro, E.)
(…) Current models of viral evolution take into account more realistic scenarios that consider compensatory and lethal mutations, a highly redundant genotype-to-phenotype map, rough fitness landscapes relating phenotype and fitness, and where phenotype is described as a set of interdependent traits. Further, viral populations cannot be understood without specifying the characteristics of the environment where they evolve and adapt. Altogether, it turns out that the pathways through which viral quasispecies go extinct are multiple and diverse.
Lethal mutagenesis and evolutionary epidemiology (by Martin, G., Gandon, S.)
The lethal mutagenesis hypothesis states that within-host populations of pathogens can be driven to extinction when the load of deleterious mutations is artificially increased with a mutagen, and becomes too high for the population to be maintained. (…) We derive the epidemiological and evolutionary equilibrium of the system. At this equilibrium, the density of the pathogen is expected to decrease linearly with the genomic mutation rate U. We also provide a simple expression for the critical mutation rate leading to extinction. Stochastic simulations show that these predictions are accurate for a broad range of parameter values. As they depend on a small set of measurable epidemiological and evolutionary parameters, we used available information on several viruses to make quantitative and testable predictions on critical mutation rates. In the light of this model, we discuss the feasibility of lethal mutagenesis as an efficient therapeutic strategy.
The fitness effects of mutations are central to evolution, yet have begun to be characterized in detail only recently. Site-directed mutagenesis is a powerful tool for achieving this goal, which is particularly suited for viruses because of their small genomes. Here, I discuss the evolutionary relevance of mutational fitness effects and critically review previous site-directed mutagenesis studies. The effects of single-nucleotide substitutions are standardized and compared for five RNA or single-stranded DNA viruses infecting bacteria, plants or animals. (…)