Faculty Spotlight


Peter Nonacs

I am interested in all sorts of biological questions from animal behavior to disease ecology. Recently I have become very interested in the paradox of diseases. If infectious disease is usually caused by organisms with very simple genomes consisting of relatively few genes, how can they overwhelm the complex and redundant immune systems of vertebrates, such as humans? One potential explanation is that genetically different disease organisms positively interact with each other to increase their group-level reproduction, through a process we have dubbed "social heterosis." In genetics, heterosis refers to hybrid vigor or the increased fitness due to outbreeding, when lineages cross that combine fitness benefits in offspring that were previously limited to each lineage. In social heterosis, different disease lineages interact as if they were multiple chromosomes rather than competing genomes in a way that enhances the growth rate of all. We tested this hypothesis by mathematically simulating HIV evolving with social heterosis within a hypothetical infected human host. Our model successfully reproduced many observed in vivo patterns of infection and transmission of HIV that previously seemed paradoxical and inexplicable. A potential practical benefit of understanding a "social genome" model of disease- host interaction is that our research could lead to novel approaches to the prevention and management of HIV and perhaps a variety of other diseases.

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