I am an evolutionary biologist and I have focused my career in using an evolutionary approach to understand host-microbe interactions. Throughout my career, I have studied how the ecological context, both in-vitro and in-vivo, affects adaptation and phenotypic-strategies of malaria parasites (Plasmodium) and commensal bacteria (Escherichia coli). During my PhD (University of Edinburgh, UK), I worked with Dr. Sarah Reece and took an evolutionary ecology approach to understand how rodent malaria parasites modulate their phenotypes in response to the ecological context. I showed that: (a) malaria parasites adapt their reproductive strategies in response to particular immune factors. This minimizes fitness declines under immune pressure (Ramiro 2011 PLoS Pathog); (b) interactions in mixed-species infections, mediated by resource availability, can turn an avirulent species into deadly one - i.e. virulence is highly dependent on the within-host ecology (Ramiro 2016 Ecol Let); (c) Plasmodium gametes express fast-evolving genes that are key for pre-zygotic isolation. Expression of these genes, which are vaccine targets, strongly reduces the formation of hybrids in mixed-species mating groups (Ramiro 2015 Proc Roy Soc B); (d) As my work benefited from a strong phylogenetic framework, I aimed to better understand the phylogeny of rodent malaria parasites - this led us to redefine the species and subspecies of this parasite group (Ramiro 2012 BMC Evol Biol). More generally, I also contributed towards a better integration of evolutionary theory with the observations made by parasitologists and molecular biologists (Reece 2009 Evol App).
To further improve on my PhD training, I joined Dr. Isabel Gordo's Lab (Instituto Gulbenkian de Ciência), where I have been taking an evolutionary genetics approach to understand the evolutionary dynamics and the genetic and phenotypic adaptations of E. coli in response to interactions with the immune system and with the complex ecosystem of the mouse gut microbiota. This work has already led me to two key insights: (a) in-vitro adaptation of E. coli to macrophages leads to significant increases in virulence in a mouse model (Miskinyte 2013 PLoS Pathog); (b) small colony variants (SCVs) are a key conserved phenotype, which emerges in the interaction with macrophages, but that is underpinned by a diverse genetic basis (Ramiro 2016 Evol App). While SCVs emerge in the interaction with macrophage, these acquire increased resistance to aminoglycoside antibiotics, but increased sensitivity to antibiotics of other classes. These observations have medical implications, as this phenotype is commonly found in natural infections. Currently, I am studying the long-term adaptation (1 year) of E. coli to the mouse gut, in the absence of antibiotics. During this study I have found that bacteria with high-mutation rates (mutators) emerge and rise in frequency. Because mutation rates are key to understand adaptation, I now wish to understand how this increased mutation rate can affect both the adaptation of bacterial populations and what are the consequences that this may bring for how E. coli interacts with its host and with other members of the gut microbiota.