Virus-host coevolution, killing the winner, and the Red Queen
نویسنده
چکیده
Viruses are the most abundant replicating entities on Earth, with an estimated 1030 virus particles in Earth's oceans alone (Suttle, 2005). Viruses play an important role in the marine carbon cycle, by viral mortality effects on the food web and by the `viral shunt' of material from higher to lower trophic levels (Fuhrman, 1999). Understanding the ecological and evolutionary interactions between viruses and their hosts is thus an important challenge if we are to understand the marine ecosystem and the global carbon cycle. Viruses are obligate parasites that replicate by taking control of infected cells and forcing them to create new virus particles, which are released during cell lysis. Each lysis (cell burst) event may release ~101102 new virus particles. Growth rate asymmetries and time-lags during viral infection mean that virus-host population dynamics are hard to model as a standard predator-prey interaction. Furthermore, population-based and analytical approaches to modelling host-virus coevolution are problematic due to massive viral diversity and rapid evolution. Here I describe a novel individual-based simulation model of host-virus coevolution in a spatial aquatic environment. Individual host cells grow at a density-dependent rate up to a parameterised carrying capacity. Virus particles may adsorb to and infect host cells with which they come into contact. After a latent period during which virus particles are replicated inside an infected cell, lysis of the infected cell releases a large number of new virus particles into the environment. This asymmetric and timelagged interaction results in boom-bust cycles of virus and host abundance, in which uninfected host populations grow until they are infected and destroyed, with associated exponential growth and collapse of viral abundance. To explore virus-host coevolution, the model focuses on the process of adsorption, in which virus tail-fibres bind to nutrient uptake receptors on the cell surface, allowing viral DNA to be injected into the cell. The `fit' between receptors and tail-fibres is thus an important locus for coevolution. The model represents this interaction in abstract form using evolvable bit-strings that represent nutrient uptake receptor configuration of host cells and tail-fibre orientation of viruses; infection occurs when these bit-strings match. This creates a coevolutionary pursuit in which hosts evolve novel strings to avoid infection, while viruses evolve strings that match their host. The need for host nutrient uptake receptors to fulfil their primary function of nutrient acquisition limits the ability of hosts to evade viral attack and creates an evolutionary trade-off between growth rate maximisation and defence. Results from the model support and quantify a theoretical prediction known as the `kill-thewinner' hypothesis (Thingstad et al, 1997), in which hosts that become abundant due to uptake efficiency become targets of viral attack. This negative density-dependent selection leads to increased host diversity. The coevolutionary dynamics of the model are characteristic of the well known `Red Queen' effect (Van Valen, 1973), whereby both viruses and hosts show continual evolutionary adaptation while maintaining broad constancy in relative fitness. Interestingly, the Red Queen effect is most pronounced in abundant host populations, while scarce host populations can achieve progressive fitness increase by improving uptake efficiency until they reach a critical abundance at which viral mortality becomes significant.
منابع مشابه
Running with the Red Queen: host-parasite coevolution selects for biparental sex.
Most organisms reproduce through outcrossing, even though it comes with substantial costs. The Red Queen hypothesis proposes that selection from coevolving pathogens facilitates the persistence of outcrossing despite these costs. We used experimental coevolution to test the Red Queen hypothesis and found that coevolution with a bacterial pathogen (Serratia marcescens) resulted in significantly ...
متن کاملHuman Virome
Viruses are dominant entities in the biosphere and parasitize all cellular life forms. The relative abundances of different classes of viruses are dramatically different between prokaryotes and eukaryotes. In marine, soil and animal-associated environments, virus particles consistently outnumber cells by one to two orders of magnitude. It is estimated that 10 quintillion (1030) viral particles ...
متن کاملHost-parasite Red Queen dynamics with phase-locked rare genotypes
Interactions between hosts and parasites have been hypothesized to cause winnerless coevolution, called Red Queen dynamics. The canonical Red Queen dynamics assume that all interacting genotypes of hosts and parasites undergo cyclic changes in abundance through negative frequency-dependent selection, which means that any genotype could become frequent at some stage. However, this prediction can...
متن کاملEcological and Evolutionary Oscillations in Host-Parasite Population Dynamics, and The Red Queen
In a host-parasite system, the constitutive interaction among the species, regulated by the growth rates and functional response, may induce populations to approach equilibrium or sometimes to exhibit simple cycles or peculiar oscillations, such as chaos. A large carrying capacity coupled with appropriate parasitism effectiveness frequently drives long-term apparent oscillatory dynamics in popu...
متن کاملA Matching-Allele Model Explains Host Resistance to Parasites
The maintenance of genetic variation and sex despite its costs has long puzzled biologists. A popular idea, the Red Queen Theory, is that under rapid antagonistic coevolution between hosts and their parasites, the formation of new rare host genotypes through sex can be advantageous as it creates host genotypes to which the prevailing parasite is not adapted. For host-parasite coevolution to lea...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
دوره شماره
صفحات -
تاریخ انتشار 2010