Climate drivers, host identity and fungal endophyte infection determine virus prevalence in a grassland ecosystem

Under climate change, alterations to precipitation and temperature regimes are expected to impact ecosystem structure and function. These impacts may in part be determined by feedbacks between plants and associated microbes, including both endophytic fungal symbionts and viral pathogens. To test potential key components of these feedbacks in a grassland system, we conducted a field experiment that factorially manipulated temperature regime, precipitation regime and endophyte infection of a dominant species, Schedonorus arundinaceus. After one growing season, we evaluated the four most frequently occurring grass species for infection by three species of barley and cereal yellow dwarf viruses (B/CYDVs). For S.arundinaceus, we also tracked changes in viral prevalence over an additional two growing seasons, for a total of three growing seasons. Plant species identity played a strong role in determining virus prevalence; Poa pratensis and Paspalum dilatatum were more frequently infected than either S.arundinaceus (endophyte infected or endophyte free) or Eleusine indica. Both elevated temperature and elevated precipitation impacted virus prevalence, but effects varied among years and interacted with fungal endophyte symbiosis for S.arundinaceus. In the final year of data collection, elevated precipitation increased virus prevalence in endophyte-infected, but not endophyte-free, S.arundinaceus. In the same year, but regardless of endophyte infection, elevated temperature by itself increased virus prevalence for S.arundinaceus. This effect of temperature on virus prevalence may have been driven by vector abundance because the viruses are obligately aphid-transmitted, and aphids were found more frequently in heated plots. Synthesis. Overall, our investigation experimentally demonstrates strong combined impacts of biotic and abiotic factors on disease dynamics in a grassland system. Impacts of climate change on virus prevalence in grasslands may depend on the responses of aphid vectors and the presence of endophytic fungal symbionts.