Pathogens can promote host diversity in a broad range of host-pathogen interaction, and it has also been seen in fungus-virus systems. Many fungi species have an allorecognition system called Vegetative-Compatibility system (VC system), and it is believed to act against viral infection. When genetically different fungal colonies contact, each fungal colony recognizes non-self and leads to cell death, resulting in limited cellular cytoplasm (virus) mixing. High diversity of VC type works as a beneficial "social distancing" strategy for fungi to reduce virus infection. On the other hand, this incompatibility makes it impossible for genetically different fungal colonies to share nutrients and living space, leading to inter-strain competition among these colonies. Because of this complicated inter- and intra-specific interaction, the theoretical mechanisms have been unknown as to whether virus infection promotes fungal genetic diversity or not, and how many VC types can coexist in nature.
To answer the two questions above, we construct a simple fungus-virus epidemiological model. Our model combines ecological interaction (competition between VC types) with epidemiological interaction (viruses infect fungi). We assume that virus infection rate between the same VC type individuals is higher than between different ones because of the VC system (due to the "social distancing" strategy).
Our model shows that the coexistence of multiple VC types is possible and that it is determined by the balance between efficiency of the VC system and strength of competition between different VC types. We have analytically derived the criteria of novel VC type invading the resident fungal population and derived the number of coexisting VC types. This research shows a new mechanism of host diversification driven by pathogen selection. We believe that it contributes to our fundamental comprehension of the evolutionary mechanism of fungus-virus interaction.