Research
We study how environmental drivers and genetic factors impact disease outcomes within and across host species. We use a model system - Caenorhabditis nematodes and Orsay virus - in our research. We are also learning about local nematode communities and their pathogens!
Caenorhabditis and Orsay virus quick facts:
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Caenorhabditis elegans has been used as a model system in laboratory studies since the 1970s. Thus, we stand on the shoulders of giants as we add to the body of work on this organism, taking advantage of previous research and well developed tools and methods.
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C. elegans eat bacteria. In the wild, they can be found in compost or rotting plant material. In the lab, they live in petri dishes filled with media.
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Orsay virus was discovered in France in 2011 by the lab of Marie-Anne Felix. It is still the only known natural virus of C. elegans. It has been used in numerous studies to learn about the anti-viral immune responses of C. elegans.
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Orsay virus is environmentally transmitted through the fecal-oral route, and infects C. elegans gut cells. It generally has low pathogenicity, but virulence depends on host and virus strain.
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There are dozens of additional Caenorhabditis species, and they look really similar to C. elegans. Some of them can become infected and some of them can't. We're trying to figure out why!
Our Current Projects
Infected C. elegans imaged with fluorescence in situ hybridization for Orsay virus RNA. We are using this method to determine infection rates across host species in this study.
Effects of microbial environment on susceptibility and disease outcomes
The environment is an important modulator of disease as abiotic and biotic conditions modulate exposure rates, pathogen infectivity, and host susceptibility, as well as the ways that hosts respond to infection, which is important for infection outcomes such as pathogenicity and transmission. We are manipulating the microbial environment of our Caenorhabditis hosts during virus exposure and measuring infection rates and virulence. In our system, bacteria serves both as food and microbiome for the hosts. In this experiment, we ask if different host species have similar or different responses to the bacterial environment.
How does maternal age impact susceptibility and disease outcomes?
Some of our responses and disease outcomes are determined before we're born and are due to parental effects. We are exploring how maternal age at embryo deposition (i.e., early or late offspring) impacts Orsay virus susceptibility, viral load, and virulence. Our experimental findings so far indicate that early offspring have more severe infections than with higher viral loads and greater fitness impacts than infection in later offspring. Next, we plan to look into a mechanism for this effect.
C. elegans adult on a bacterial lawn with two embryos.
Does catena position impact soil nematode community structure?
Nematodes are super abundant and diverse and serve important roles in soils. There are nematode groups that feed at each soil trophic level and they are important for nutrient cycling. We aim to describe how elevational differences across a landscape structure nematode communities. Importantly, catenas (gradients down hillsides) show that soil properties and moisture content change from top to bottom. Likewise, we expect nematode communities to differ.
Gwen with a soil core from our Bagley catena.
When, why, and how often do pathogens spill over into non-reservoir hosts?
A pathogen can spill over when it encounters a new host and it can infect, evade the host's immune response, and exploit its resources. Keeping exposure doses constant, I found that closely related worm host species have similar susceptibilities to Orsay virus, likely due to similar within-host conditions (see figure to the right from Shaw & Kennedy 2022). What are the shared traits of related species that make them susceptible? We will investigate determinants of spillover in this system by examining traits (e.g. feeding rates, gut pH, population growth rates, candidate genes) and variation in susceptibility within and across species. Determining which host traits predict susceptibility will add to the value of this system for studying spillover and emergence.
