I am a viral ecologist studying the dynamics of cross-species transmission and host shifts. Much of my work takes a comparative approach, aiming to discover generalisable patterns which may help us to anticipate and prepare for future outbreaks of infectious disease.
How do vertebrates stop their sequence-specific antiviral defences from accidentally targeting their own gene transcripts? We show that self-targeting by antiviral effectors - and ZAP in particular - has shaped the composition of host transcripts in the vertebrate interferome. These unique compositional signatures give us a better picture of what viral genomes capable of evading sequence-specific host defences might look like, an observation we are exploiting in our work to develop genome-based zoonotic risk prediction methods.
Why most cross-species transmissions fail to establish ongoing transmission in the newly infected species remains poorly understood. Examining cross-species inoculations involving rabies, we show that mismatches in virulence which are predictable from host and viral factors make sustained transmission in the novel host less likely. These mechanistic insights help to explain and predict host shift events and highlight meta-analyses of existing experimental inoculation data as a powerful and generalisable approach for understanding the dynamics of index infections in novel species.
Do some reservoir groups (e.g. bats) produce more zoonotic viruses than others? By cataloguing the accepted reservoirs for 415 viruses associated with mammals and birds, we show that there is currently no evidence for the existance of any such special reservoir groups. Instead, groups containing more reservoir species are associated with more viruses, and proportionally more zoonotic viruses.