Presently I hold an Academy Research Fellowship at the University of Helsinki. My project concentrates on analysing the role of ecological processes in affecting the interaction between environmental opportunistic pathogens (by these I mean organisms that live freely in the environment, but are able to infect host individuals upon contact) and their hosts. This work combines both theoretical analysis and microcosm experiments.

Previously, I worked as a post-doctoral fellow in a project lead by prof. Ilkka Hanski (
✝ 2016). This project concentrates on highlighting the role of the living environment on the development of atopic sensitisation in children. This work also includes analysis of the composition human microbiota and how this might relate to the regulation of the immune function. After prof. Hanski passed away, I have been in charge of this project.

After finnishing my PhD thesis and doing a short postdoc with Peter Abrams in Toronto, I started a project (postdoctoral research project, funded by the Academy of Finland) dealing with integrating spatial and temporal environmental variation in models of ecological communities. While my main research involved analysing stochastic community models, I also collaborated in research projects dealing with ecotoxicological consequences of heavy metals on chironomid communites and their bat predators, as well as testing and developing numerical methods for empirical community ecology.

My research interests include:

Community ecology
Interspecific interactions
Environmental stochasticity
– Disease ecology
– N
umerical ecology.

Past activities

2013–2015 Postdoctoral fellow in the Metapopulation Researcg Group with prof. Ilkka Hanski.

2011–2013 Postdoctoral research project funded by the Academy of Finland, considering the role of spatio-temporal environmental variation on the dynamics of metacommunities.

In 2010 I worked as a postdoctoral fellow at the university of Turku, Finland, in the project of prof. Kai Norrdahl dealing with the predictability of food web composition.

In 2009–2010 I worked at the University of Toronto, under the supervision of professors Peter Abrams & Brian Shuter, also collaborating with prof. Kevin McCann (U of Guelph). This work in Toronto dealt with food web models and the influence of climate change on spatially coupled food chains.

I did my PhD in the University of Helsinki, working in the Integrative Ecology Group, under the supervision of profs. Esa Ranta (✝ 2008) and Veijo Kaitala, and Dr. Mike Fowler. My thesis concentrated around ecological communities and the impact of environmental stochasticity on biological systems in general.

Monday, 17 October 2016

A mechanistic underpinning for sigmoid dose-dependent infection

Sigmoidal, dose-dependent infection: theoretical & empirical justification 

It has been proposed that biodiversity loss leads to reduced interaction between environmental and human microbiotas. Theoretical models of environmentally transmitted diseases often assume that transmission is a constant process, which scales linearly with pathogen dose. Here we question the applicability of such an assumption and propose a sigmoidal form for the pathogens infectivity response. In our formulation, this response arises under two assumptions: 1) multiple invasion events are required for a successful pathogen infection and 2) the host invasion state is reversible. The first assumption reduces pathogen infection rates at low pathogen doses, while the second assumption, due to host immune function, leads to a saturating infection rate at high doses. The derived pathogen dose:infection rate -relationship was tested against an experimental data on host mortality rates across different pathogen doses. Compared to two simpler alternatives, the sigmoidal function gave a better fit to patterns in host mortality rate (process), as well as host mortality (endpoint). Combining these alternative approaches made us more confident to conclude that the proposed model for disease transmission is theoretically sound, provides a good description of the data at hand, and is likely to be useful in developing more reliable models for infectious diseases.

A schematic illustration of a potential mechanism that gives arise to a sigmoidal infection response. In this model, each invading pathogen (with rate αP) moves the host towards the state Sn, from which the host may acquire an infection (with rate γ). Before an infection is acquired, the host immune system clears the invading pathogens (with rate β). A sigmoidal rate of infection formation requires that n > 2. See more details in: A mechanistic underpinning of sigmoid dose-dependent infection.

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