Samuel ALIZON

Research interests

Here are some of the projects I am currently invested in along with links to reviews I contributed to. Many (if not most) of these projects are collaborations.

Evolutionary epidemiology - Infectious diseases evolve as they spread
Microparasites (i.e. viruses, bacteria, protozoa) evolve rapidly. As a consequence, strains found late in an epidemics can have little in common with the original strain. I am interested in introducing evolutionary theory in epidemiology in order to better understand the spread of infectious diseases. In particular, I study the feedbacks between epidemiology and disease evolution: the epidemiology shapes disease evolution and how, in return, disease evolution affects the epidemiology.
Virulence evolution - Why do parasites harm their host?
In most cases, killing the host seems like a waste because it shortens the duration of the infection. I develop mathematical models to understand the evolutionary constraints that lead to the emergence and the persistence of virulent strains. Some of these constraints are trade-offs between epidemiological traits (virulence, transmission, recovery), but also more ecological processes such as multiple infections. For a review, see Alizon et al. (2009) J. Evol. Biol.
Nested models - Describing the underlying mechanisms of an infection.
Nested models combine an explicit modeling of within-host processes and an epidemiological framework. These models can be used to study the mechanistic bases of epidemiological trade-offs or to consider cases where within-host and between-host dynamics overlap (which is the case for instance for rapidly evolving diseases). For a review, see Mideo et al. (2008) Trends Ecol. Evol.
Rapidly evolving diseases - Evolutionary dynamics in a host.
Some parasites, such as HIV or hepatitis C virus (HCV), have so short generation times that evolution actually occurs over the course of an infection. I study the implications of within-host evolution at two levels. First, at the level of an infection, how does within-host evolution explain the course of the disease? This involves a combination of models of cell population dynamics and parasite evolution. Second, at an epidemiological level, how is the rapid adaptation to a host going to affect the way a disease spreads in a host population? I develop both conceptual models and data-driven analyses on HIV and HCV. A review is in preparation (contact me)
Multiple infections and disease evolution - Several strains sharing a host.
Very often a host is not infected by a single parasite genotype but by two (or more) genotypes. This leads to a co-infection. Co-infections generate a conflict between levels of selection because the optimal parasite strategy to spread among hosts is not necessarily the same as the optimal strategy within a host. Also, many biological interactions can occur within a host and parasites from different strains can cooperate or compete.
I develop epidemiological and nested models to understand how co-infections affect the evolution of traits such as virulence. I also use co-infection models to develop kin selection models. The idea is to see how the relatedness between co-infecting strains affects parasite evolution. These multiple infection models have implications for parasites such as Plasmodium. A review is in preparation (contact me)
Host population structure - Adding realism to host contact patterns.
Most models in epidemiology assume that the host population is "well-mixed", i.e. that potentially all the individuals can interact. In reality, there is often a spatial structure in the population such that individuals can only interact with a subset of the population. For instance, in the case of sexually transmitted diseases, studies are able to infer the structure of the host population (i.e. the distribution of the number of partners per individual), which greatly affects the way diseases spread and evolve.

Other topics I am interested in:

Evolution of vector-borne diseases: Many parasites, such as Plasmodium (which is responsible for malaria) are transmitted by a vector. This creates very specific constraints on parasite evolution. It raises additional issues linked to multiple infections or within-host evolution. For a review on plant viruses, see Froissart et al. (2010) Phil. Trans. R. Soc. Lond.
Darwinian medicine: This field has been popularized since the 1990s. The idea is to use evolutionary medicine to fight diseases in general (not only infectious diseases). I am interested in understanding whether there is indeed a new field or only a heteroclitic assemblage.
Evolutionary consequences of public health policies: Large scale public health policies such as vaccination or drug treatment create strong selective pressures on parasites. One of the aims of my work is to better understand (and predict) parasite evolutionary responses to specific public health policies in order for instance to avoid an arms race between parasites and hosts.
Modelling within-host dynamics: Through the development of nested models, I got interested in models of within-host dynamics, especially immune dynamics. More specifically, I ask how far can we make parallels with ecological models. For a review, see Alizon & van Baalen (2008) Am. Nat.

For further details, please contact me or see my publication list.

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