Background/Question/Methods Despite its importance for human and animal health, the ecology and evolution of infectious disease emergence is critically understudied from an empirical perspective because thus far, there has not been an animal laboratory system in which host ecology can be manipulated and the consequences for evolution of emergence observed. This type of study would require large, easy-to-manipulate host populations and a naturally transmitting pathogen that can rapidly evolve the ability to transmit among novel hosts. Here, we present our progress developing such a system: Caenorhabditis nematode hosts and the gut pathogen Orsay virus, the only known native virus of C. elegans. Using a panel of 40 Caenorhabditis nematode species, we are assaying the susceptibility of host species to Orsay virus by exposing hosts to the virus using the natural route of transmission. After we allowed the virus to transmit and replicate within host populations, we quantified virus by qPCR. In species with evidence of virus infection, we tested for virus transmission by passaging five nematodes from virus-exposed populations to virus-free media where nematodes seed new populations and have the potential to transmit virus. Results/Conclusions We have found that 12 of 40 novel host species amplify Orsay virus to levels well above exposure doses, indicating that they are susceptible to the virus. In 13 of 17 species where the susceptibilities of multiple strains have been assayed, strains yielded qualitatively similar results. Continued assays will allow us to determine if susceptibility to Orsay virus is a species-level trait or if susceptibility varies within species across the Caenorhabditis tree. In contrast to expected patterns, we have so far found no relationship between susceptibility to Orsay virus and phylogenetic relatedness. We have also found that the susceptible hosts C. wallacei, C. latens, C. sulstoni, C. macrosperma, and C. tropicalis do not transmit virus to conspecifics as readily as transmission occurs in populations of the native C. elegans, despite amplifying virus to comparable levels. These features make the system a compelling one to study virus emergence, since the virus is able to replicate within novel host species, but it needs to evolve to persist within populations of these hosts. We aim to use this system to determine what ecological conditions influence the ability of viruses to evolve from non-sustained spillover (R0<1) to endemic disease (R0>1) in novel host populations.
