Sobre el estudio de la evolución

Hace una semana salió publicado en la revista Science un artículo sobre abejas, diversidad y el origen de la poliandria en la naturaleza. Me resultó muy llamativo, sobre todo por el título. Cualquiera que trabaje con evolución de virus verá que este artículo no puede dejarnos indiferentes. El artículo en cuestión es:

Science. 2007 Jul 20;317(5836):362-4.
Genetic diversity in honey bee colonies enhances productivity and fitness.
Mattila HR, Seeley TD.
Department of Neurobiology and Behavior, Cornell University, Ithaca, NY 14853, USA. hrm24@cornell.edu
Honey bee queens mate with many males, creating numerous patrilines within colonies that are genetically distinct. The effects of genetic diversity on colony productivity and long-term fitness are unknown. We show that swarms from genetically diverse colonies (15 patrilines per colony) founded new colonies faster than swarms from genetically uniform colonies (1 patriline per colony). Accumulated differences in foraging rates, food storage, and population growth led to impressive boosts in the fitness (i.e., drone production and winter survival) of genetically diverse colonies. These results further our understanding of the origins of polyandry in honey bees and its benefits for colony performance.

¿Qué ocurre cuando disminuimos la diversidad de un virus aumentando, por ejemplo, la fidelidad de la enzima que copia su genoma? Esto fue publicado por el grupo de Karla Kirkegaard en PLoS Pathog hace un par de años:

PLoS Pathog. 2005 Oct;1(2):e11. Epub 2005 Oct 7.
Increased fidelity reduces poliovirus fitness and virulence under selective pressure in mice.
Pfeiffer JK, Kirkegaard K.
Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California, USA.
RNA viruses have high error rates, and the resulting quasispecies may aid survival of the virus population in the presence of selective pressure. Therefore, it has been theorized that RNA viruses require high error rates for survival, and that a virus with high fidelity would be less able to cope in complex environments. We previously isolated and characterized poliovirus with a mutation in the viral polymerase, 3D-G64S, which confers resistance to mutagenic nucleotide analogs via increased fidelity. The 3D-G64S virus was less pathogenic than wild-type virus in poliovirus-receptor transgenic mice, even though only slight growth defects were observed in tissue culture. To determine whether the high-fidelity phenotype of the 3D-G64S virus could decrease its fitness under a defined selective pressure, we compared growth of the 3D-G64S virus and 3D wild-type virus in the context of a revertible attenuating point mutation, 2C-F28S. Even with a 10-fold input advantage, the 3D-G64S virus was unable to compete with 3D wild-type virus in the context of the revertible attenuating mutation; however, in the context of a non-revertible version of the 2C-F28S attenuating mutation, 3D-G64S virus matched the replication of 3D wild-type virus. Therefore, the 3D-G64S high-fidelity phenotype reduced viral fitness under a defined selective pressure, making it likely that the reduced spread in murine tissue could be caused by the increased fidelity of the viral polymerase.


¿Y qué pasa si un virus pierde su capacidad de diversificarse? ¿Y si se restaura esta capacidad de manera artificial? El año pasado, el grupo de Raul Andino contestó esta pregunta empleando poliovirus y su neurotropismo.

Nature. 2006 Jan 19;439(7074):344-8. Epub 2005 Dec 4.
Quasispecies diversity determines pathogenesis through cooperative interactions in a viral population.
Vignuzzi M, Stone JK, Arnold JJ, Cameron CE, Andino R.
Department of Microbiology and Immunology, University of California, San Francisco, California 94143-2280, USA.
An RNA virus population does not consist of a single genotype; rather, it is an ensemble of related sequences, termed quasispecies. Quasispecies arise from rapid genomic evolution powered by the high mutation rate of RNA viral replication. Although a high mutation rate is dangerous for a virus because it results in nonviable individuals, it has been hypothesized that high mutation rates create a 'cloud' of potentially beneficial mutations at the population level, which afford the viral quasispecies a greater probability to evolve and adapt to new environments and challenges during infection. Mathematical models predict that viral quasispecies are not simply a collection of diverse mutants but a group of interactive variants, which together contribute to the characteristics of the population. According to this view, viral populations, rather than individual variants, are the target of evolutionary selection. Here we test this hypothesis by examining the consequences of limiting genomic diversity on viral populations. We find that poliovirus carrying a high-fidelity polymerase replicates at wild-type levels but generates less genomic diversity and is unable to adapt to adverse growth conditions. In infected animals, the reduced viral diversity leads to loss of neurotropism and an attenuated pathogenic phenotype. Notably, using chemical mutagenesis to expand quasispecies diversity of the high-fidelity virus before infection restores neurotropism and pathogenesis. Analysis of viruses isolated from brain provides direct evidence for complementation between members in the quasispecies, indicating that selection indeed occurs at the population level rather than on individual variants. Our study provides direct evidence for a fundamental prediction of the quasispecies theory and establishes a link between mutation rate, population dynamics and pathogenesis.

¿Y, finalmente, qué ocurre si los virus RNA leen a Lewis Carroll?

Proc Natl Acad Sci U S A. 1994 May 24;91(11):4821-4.
The red queen reigns in the kingdom of RNA viruses.
Clarke DK, Duarte EA, Elena SF, Moya A, Domingo E, Holland J.
Department of Biology, University of California at San Diego, La Jolla 92093-0116.
Two clonal populations of vesicular stomatitis virus of approximately equal relative fitness were mixed together and allowed to compete during many transfers in vitro as large virus populations. Eventually, one or the other population suddenly excluded its competitor population, yet both the winners and losers exhibited absolute gains in fitness. Our results agree with the predictions of two major theories of classical population biology; the Competitive Exclusion Principle and the Red Queen's Hypothesis, where (in Lewis Carroll's words) "it takes all the running you can do to keep in the same place."

¡¡¡Echan a correr!!!