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Biomedical subjects

Jean-Baptiste André

Publications and source records attributed to Jean-Baptiste André.

9 recordsLinked to original sources
PubMed2006

The evolutionary emergence of pandemic influenza.

Pandemic influenza remains a serious public health threat and the processes involved in the evolutionary emergence of pandemic influenza strains remain incompletely understood. Here, we develop a stochastic model for the evolutionary emergence of pandemic influenza, and use it to address three main questions. (i) What is the minimum annual number of avian influenza virus infections required in humans to explain the historical rate of pandemic emergence? (ii) Are such avian influenza infections in humans more likely to give rise to pandemic strains if they are driven by repeated cross-species introductions, or by low-level transmission of avian influenza viruses between humans? (iii) What are the most effective interventions for reducing the probability that an influenza strain with pandemic potential will evolve? Our results suggest that if evolutionary emergence of past pandemics has occurred primarily through viral reassortment in humans, then thousands of avian influenza virus infections in humans must have occurred each year for the past 250 years. Analyses also show that if there is epidemiologically significant variation among avian influenza virus genotypes, then avian virus outbreaks stemming from repeated cross-species transmission events result in a greater likelihood of a pandemic strain evolving than those caused by low-level transmission between humans. Finally, public health interventions aimed at reducing the duration of avian virus infections in humans give the greatest reduction in the probability that a pandemic strain will evolve.

Animals↗
PubMed2006

The evolutionary consequences of plasticity in host-pathogen interactions.

Interactions between individuals such as hosts and pathogens are often characterized by substantial phenotypic plasticity. Pathogens sometimes alter their exploitation strategies in response to defensive strategies adopted by their host and vice versa. Nevertheless, most game-theoretic models developed to explain the evolution of pathogen and host characteristics assume that no such plasticity occurs. Allowing for phenotypic plasticity in these models is difficult because one must focus on the evolution of pathogen and host reaction norms, and then allow for the potentially indefinite reciprocal changes in pathogen and host behaviour that occur during an infection as a result of their interacting reaction norms. Here, we begin to address these issues for a simple host-pathogen system in which the pathogen exhibits a level of virulence and the host exhibits a level of immune clearance. We find, quite generally, that plasticity promotes the evolution of higher levels of cooperation, in this case leading to reduced levels of both virulence and clearance.

Biological Evolution↗
PubMed2006

Within-host evolution and virulence in microparasites.

An important aspect of microparasite biology is the fact that infections are populations of thousands of microbes. As any population, infections are hence subject to two main types of changes: demographic and evolutionary. Here we analyse the consequences of within-host evolutionary changes. We build an epidemiological model where infections are regularly invaded by locally favored mutations affecting various infectious traits (virulence, transmissibility and clearance). Our results are the following. In durable infections, where within-host evolution is an important matter, a drop of transmissibility is only slightly deleterious to the infection, while a reduction of infection lifespan is very costly. In consequence, locally favored mutations reducing transmissibility reach a larger frequency, or even the complete fixation, and the suboptimality accumulated in infections owing to within-host evolution affects more their transmission than their duration. Conversely, taking an infection at random and observing the events of within-host evolution, one is more likely to observe reductions of infection length than reductions of transmissibility, because the mutations affecting transmissibility are often already present in infections. We then discuss the interpretation of these results in terms of deleterious mutations, and we also emphasize that the management of within-host evolution could be used as a novel therapeutic approach to the treatment of infection.

Animals↗
PubMed2006

Vaccination, within-host dynamics, and virulence evolution.

We explore the potential consequences of vaccination on parasite epidemiology and evolution. Our model combines a microscopic (within-host dynamics) and a macroscopic (epidemiological dynamics) description of the interaction between the parasite and its host. This approach allows relevant epidemiological traits such as parasite transmission, parasite virulence, and host recovery to emerge from a mechanistic model of acute infection describing the interaction between the parasite and the host immune system. We model the effect of a vaccine as an activator of immunity enhancing the replication rate of lymphocytes, their initial density at infection's initiation, their efficacy to kill the parasite, or their activation delay after infection. We analyze the evolution of the replication rate of parasites and show that vaccination may promote the evolution of faster replicating and, consequently, more virulent strains. We also show that intermediate vaccination coverage may lead to the coexistence of two different parasite strategies (a low-virulence strain adapted to naive hosts, and a high-virulence strain, more generalist, adapted to both naive and vaccinated hosts). We discuss the consequences of various vaccination strategies under different epidemiological situations using several distinct measures to evaluate the cost induced by the parasite on individuals and entire host populations.

Animals↗
PubMed2005

The effect of disease life history on the evolutionary emergence of novel pathogens.

We present a general analytical result for the probability that a newly introduced pathogen will evolve adaptations that allow it to maintain itself within any novel host population, as a function of disease life-history parameters. We demonstrate that this probability of "evolutionary emergence" depends on two key properties of the disease life history: (i) the basic reproduction number and (ii) the expected duration of an infection. These parameters encapsulate all of the relevant information and can be combined in a very simple expression, with estimates for the rates of adaptive mutation, to predict the probability of emergence for any novel pathogen. In general, diseases that initially have a large reproductive number and/or that cause relatively long infections are the most prone to evolutionary adaptation.

Adaptation, Physiological↗
PubMed2005

The evolution of mutation rate in finite asexual populations.

In this article, we model analytically the evolution of mutation rate in asexual organisms. Three selective forces are present. First, everything else being equal, individuals with higher mutation rate have a larger fitness, thanks to the energy and time saved by not replicating DNA accurately. Second, as a flip side, the genome of these individuals is replicated with errors that may negatively affect fitness. Third, and conversely, replication errors have a potential benefit if beneficial mutations are to be generated. Our model describes the fate of modifiers of mutation rate under the three forces and allows us to predict the long-term evolutionary trajectory of mutation rate. We obtain three major results. First, in asexuals, the needs for both adaptation and genome preservation are not evolutionary forces that can stabilize mutation rate at an intermediate optimum. When adaptation has a significant role, it primarily destabilizes mutation rate and yields the emergence of strong-effect mutators. Second, in contrast to what is usually believed, the appearance of modifiers with large mutation rate is more likely when the fitness cost of each deleterious mutation is weak, because the cost of replication errors is then paid after a delay. Third, in small populations, and even if adaptations are needed, mutation rate is always blocked at the minimum attainable level, because the rate of adaptation is too slow to play a significant role. Only populations whose size is above a critical mass see their mutation rate affected by the need for adaptation.

Adaptation, Physiological↗
PubMed2005

Virulence evolution in emerging infectious diseases.

Models of virulence evolution generally consider the outcome of competition between resident and mutant parasite strains at or near endemic equilibrium. Less studied is what happens during the initial phases of invasion and adaptation. Understanding initial adaptive dynamics is particularly important in the context of emerging diseases in wildlife and humans, for which rapid and accurate intervention may be of the essence. To address the question of virulence evolution in emerging diseases, we employ a simple stochastic modeling framework. As is intuitive, the pathogen strains most likely to emerge are those with the highest net reproductive rates (R0). We find, however, that stochastic events shape the properties of emerging pathogens in sometimes unexpected ways. First, the mean virulence of emerging pathogens is expected to be larger in dense host populations and/or when transmission is high, due to less restrictive conditions for the spread of the pathogen. Second, a positive correlation between average virulence and transmissibility emerges due to a combination of drift and selection. We conclude that at least in the initial phases of adaptation, special assumptions about constraints need not be invoked to explain some virulence-transmission correlations and that virulence management practices should consider how residual variation in transmission and virulence can be selected to reduce the prevalence and/or virulence of emerging infectious diseases.

Biological Evolution↗
PubMed2003

Within-host parasite dynamics, emerging trade-off, and evolution of virulence with immune system.

Virulence is an evolutionary paradox because parasites never benefit from their host's death. The adaptive explanation of virulence is classically based upon the existence of physiological constraints that create a trade-off between parasites' epidemiological traits (virulence, transmissibility, and clearance). Here we develop an epidemiological model where infections are dynamic processes and we demonstrate how these dynamics generate a trade-off between emerging epidemiological parameters. We then study how host's immune strength modifies this trade-off and hence influences virulence evolution. We found that in acute infections, where parasites are engaged in a race with immune cells, immunity restrains more the duration of the infection than its intensity. As a consequence parasites evolve to provoke more virulent but shorter infections in strongly immunized hosts.

Biological Evolution↗