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RESEARCH PRODUCT
The role of spatial structure in the evolution of viral innate immunity evasion: A diffusion-reaction cellular automaton model
Rafael SanjuánErnesto Segredo-oterosubject
0301 basic medicinePhysiologyApoptosisVirus ReplicationBiochemistryVirionsEpitopes0302 clinical medicineInterferonMedicine and Health SciencesBiology (General)Innate Immune Systemeducation.field_of_studyCell DeathEcology3. Good healthCell biologyPhenotypeComputational Theory and MathematicsCell ProcessesModeling and SimulationViral evolutionHost-Pathogen InteractionsVirusesSignal TransductionResearch Articlemedicine.drugEvolutionary ImmunologyQH301-705.5ImmunologyPopulationViral StructureBiologyAntiviral AgentsMicrobiologyViral EvolutionVirusViral Proteins03 medical and health sciencesCellular and Molecular NeuroscienceImmunityVirologyGeneticsmedicineAnimalsHumansComputer SimulationSocial BehavioreducationMolecular BiologySecretionEcology Evolution Behavior and SystematicsImmune EvasionEvolutionary BiologyInnate immune systemVirionBiology and Life SciencesProteinsCell BiologyEvasion (ethics)Immunity InnateOrganismal Evolution030104 developmental biologyViral replicationImmune SystemMicrobial EvolutionInterferonsPhysiological Processes030217 neurology & neurosurgerydescription
Most viruses have evolved strategies for preventing interferon (IFN) secretion and evading innate immunity. Recent work has shown that viral shutdown of IFN secretion can be viewed as a social trait, since the ability of a given virus to evade IFN-mediated immunity depends on the phenotype of neighbor viruses. Following this idea, we investigate the role of spatial structure in the evolution of innate immunity evasion. For this, we model IFN signaling and viral spread using a spatially explicit approximation that combines a diffusion-reaction model and cellular automaton. Our results indicate that the benefits of preventing IFN secretion for a virus are strongly determined by spatial structure through paracrine IFN signaling. Therefore, innate immunity evasion can evolve as a cooperative or even altruistic trait based on indirect fitness effects that IFN shutdown exerts on other members of the viral population. We identify key factors determining whether evasion from IFN-mediated immunity should evolve, such as population bottlenecks occurring during viral transmission, the relative speed of cellular infection and IFN secretion, and the diffusion properties of the medium.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2020-01-01 |