Abstract
The production of large progeny numbers affected by high mutation rates is a ubiquitous strategy of viruses, as it promotes quick adaptation and survival to changing environments. However, this situation often ushers in an arms race between the virus and the host cells. In this paper we investigate in depth a model for the dynamics of a phenotypically heterogeneous population of viruses whose propagation is limited to two-dimensional geometries, and where host cells are able to develop defenses against infection. Our analytical and numerical analyses are developed in close connection to directed percolation models. In fact, we show that making the space explicit in the model, which in turn amounts to reducing viral mobility and hindering the infective ability of the virus, connects our work with similar dynamical models that lie in the universality class of directed percolation. In addition, we use the fact that our model is a multicomponent generalization of the Domany-Kinzel probabilistic cellular automaton to employ several techniques developed in the past in that context, such as the two-site approximation to the extinction transition line. Our aim is to better understand propagation of viral infections with mobility restrictions, e.g., in crops or in plant leaves, in order to inspire new strategies for effective viral control.
Highlights
Cellular parasites are an ineluctable outcome of the very evolutionary process [1]
The adaptive ability of RNA viruses is a consequence of the vast genetic diversity of their populations, composed by a large number of individuals that replicate their genomes at a mutation rate several orders of magnitude higher than that of cellular DNA [2]
In [27] we showed that our model of viral propagation with R states belongs to the directed percolation (DP) universality class
Summary
Cellular parasites are an ineluctable outcome of the very evolutionary process [1]. Animal and plant cells can be infected by a variety of viruses, usually with a high degree of specificity. The adaptive ability of RNA viruses is a consequence of the vast genetic diversity of their populations, composed by a large number of individuals that replicate their genomes at a mutation rate several orders of magnitude higher than that of cellular DNA [2]. The survival of RNA viruses depends, among others, on host’s ability to fight infection, on its capacity to defeat the parasite through the immune system, and on the features of the environment where infection takes place. To guarantee their survival and propagation, viruses deploy many different and complex strategies that are still poorly known. Extinction may occur through a progressive decrease in population numbers [5] or as a result of stochastic effects in small populations affected by an increasing production of defective viral forms [11,12]
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