The role of spatial heterogeneity in the evolution of local and global infections of viruses.

Koich Saeki,Akira Sasaki,Natalia L Komarova

doi:10.1371/journal.pcbi.1005952

Abstract

Viruses have two modes spread in a host body, one is to release infectious particles from infected cells (global infection) and the other is to infect directly from an infected cell to an adjacent cell (local infection). Since the mode of spread affects the evolution of life history traits, such as virulence, it is important to reveal what level of global and local infection is selected. Previous studies of the evolution of global and local infection have paid little attention to its dependency on the measures of spatial configuration. Here we show the evolutionarily stable proportion of global and local infection, and how it depends on the distribution of target cells. Using an epidemic model on a regular lattice, we consider the infection dynamics by pair approximation and check the evolutionarily stable strategy. We also conduct the Monte-Carlo simulation to observe evolutionary dynamics. We show that a higher local infection is selected as target cells become clustered. Surprisingly, the selected strategy depends not only on the degree of clustering but also the abundance of target cells per se.

Highlights

Viruses have evolved various mechanisms to spread within a host body and between hosts
Some experimental evidences support the possibility that high ability of cell-to-cell infection is selected in the host
We address what level of cell-to-cell infection is selected in different target cell distributions

Summary

Introduction

Viruses have evolved various mechanisms to spread within a host body and between hosts. There are two modes for viral spread in a host body, one is to release infectious particles (virions) from the infected cells into the extracellular medium, and the other is to infect directly from an infected cell to an adjacent cell. Viruses that lyse the host cell rely on the release of virions as the only way of spreading. The simplest mechanism of cell-to-cell spread is the fusion of infected and uninfected cells. To enter into a host cell, some viruses have proteins that cause membrane fusion, and these fusion proteins are expressed on the cell surface after viral replication is initiated. Influenza virus have the potential to spread in a cell-to-cell manner but inherently release virions [3,4]. Other more sophisticated mechanisms of cell-to-cell virus spread exist (for more examples, see [5])

Objectives

Results

Discussion

Conclusion