Visiting Sick People: Is It Really Detrimental to Our Health?

Intuitively, keeping ones distance from a source of infection would appear to be the best way to limit the occurrence of disease. However, this overlooks the importance of repeated infections in maintaining efficient immune defenses. When acquired immunity has partly waned, re-exposure to the pathogenic agent may lead to mild disease that boosts the immune system. This prevents the total loss of immunity that would lead to classical disease in cases of re-infection. Here, using a mathematical model, we show that avoiding the pathogenic agent is detrimental in some situations, e.g. for pathogens that are highly transmissible, are not excessively lethal and that induce rapidly waning immunity. Reducing exposure to pathogenic agents is among the objectives of most, if not all, public health measures. A better understanding of the factors influencing the severity of a disease is required before applying measures that reduce the circulation of pathogenic agents

Emergence and Prevalence of Human Vector-Borne Diseases in Sink Vector Populations

Vector-borne diseases represent a major public health concern in most tropical and subtropical areas, and an emerging threat for more developed countries. Our understanding of the ecology, evolution and control of these diseases relies predominantly on theory and data on pathogen transmission in large self-sustaining ‘source’ populations of vectors representative of highly endemic areas. However, there are numerous places where environmental conditions are less favourable to vector populations, but where immigration allows them to persist. We built an epidemiological model to investigate the dynamics of six major human vector borne-diseases in such non self-sustaining ‘sink’ vector populations. The model was parameterized through a review of the literature, and we performed extensive sensitivity analysis to look at the emergence and prevalence of the pathogen that could be encountered in these populations. Despite the low vector abundance in typical sink populations, all six human diseases were able to spread in 15–55% of cases after accidental introduction. The rate of spread was much more strongly influenced by vector longevity, immigration and feeding rates, than by transmission and virulence of the pathogen. Prevalence in humans remained lower than 5% for dengue, leishmaniasis and Japanese encephalitis, but substantially higher for diseases with longer duration of infection; malaria and the American and African trypanosomiasis. Vector-related parameters were again the key factors, although their influence was lower than on pathogen emergence. Our results emphasize the need for ecology and evolution to be thought in the context of metapopulations made of a mosaic of sink and source habitats, and to design vector control program not only targeting areas of high vector density, but working at a larger spatial scale

Animal health perceived in the light of ecology and evolution

Infectious diseases remain a major cause of animal mortality and morbidity. Global changes, including fragmentation of habitats of many animal species, modify the ecology of host-parasite relationships and the selection pressures on infectious agents, introducing high uncertainty about the impact and evolution of these diseases. In such a context, it is important to integrate ecology and evolutionary science to animal health issues for a better understanding and a better management of infectious diseases. From our work we illustrate the contribution of an eco-evolutionary vision of infectious diseases in animals. The first two examples illustrate the importance of including eco-evolutionary dimension to the understanding and management of infectious animal diseases. The last two sections show that, in turn, the data collected in the field can also provide fundamental knowledge on important issues that are often addressed in the laboratory. Given their complexity, these issues can only be addressed by iterating back and forth between experimental data and mathematical modelingLes maladies infectieuses demeurent une cause majeure de mortalité en santé animale. Les changements globaux, notamment la fragmentation des habitats de nombreuses espèces animales, modifient l’écologie des relations hôtes-parasites et les pressions qui s’exercent sur les agents infectieux, introduisant une importante incertitude sur l’impact et l’évolution de ces maladies. Dans un tel contexte, il est important d’intégrer les sciences de l’Écologie et de l’Évolution aux problèmes de santé animale pour une meilleure compréhension et une meilleure gestion des maladies infectieuses. Nous illustrons à partir de nos travaux les apports d’une vision éco-évolutionniste des maladies infectieuses chez l’animal. Les deux premiers exemples illustrent l’intérêt d’inclure la dimension éco-évolutive pour la compréhension et la gestion des maladies infectieuses animales. Les deux dernières parties montrent qu’en retour, les données recueillies sur le terrain peuvent également apporter une connaissance fondamentale sur des questions importantes qui sont le plus souvent abordées en laboratoire. Compte-tenu de leur complexité, ces questions ne peuvent être traitées que par des allers-retours entre données et modélisation mathématiqu

Knock-out of the Mg protoporphyrin IX methyltransferase gene in Arabidopsis: Effects on chloroplast development and on chloroplast-to-nucleus signaling.

International audienceProtoporphyrin IX is the last common intermediate between the haem and chlorophyll biosynthesis pathways. The addition of Mg directs this molecule toward chlorophyll biosynthesis. The first step downstream from the branchpoint is catalyzed by the Mg chelatase and is a highly regulated process. The corresponding product, Mg protoporphyrin IX, has been proposed to play an important role as a signaling molecule implicated in plastid-to-nucleus communication. In order to get more information on the chlorophyll biosynthesis pathway and on Mg protoporphyrin IX derivative functions, we have identified an Mg protoporphyrin IX methyltransferase (CHLM) knock-out mutant in Arabidopsis in which the mutation induces a blockage downstream from Mg protoporphyrin IX and an accumulation of this chlorophyll biosynthesis intermediate. Our results demonstrate that the CHLM gene is essential for the formation of chlorophyll and subsequently for the formation of photosystems I and II and cyt b6f complexes. Analysis of gene expression in the chlm mutant provides an independent indication that Mg protoporphyrin IX is a negative effector of nuclear photosynthetic gene expression, as previously reported. Moreover, it suggests the possible implication of Mg protoporphyrin IX methylester, the product of CHLM, in chloroplast-to-nucleus signaling. Finally, post-transcriptional up-regulation of the level of the CHLH subunit of the Mg chelatase has been detected in the chlm mutant and most likely corresponds to specific accumulation of this protein inside plastids. This result suggests that the CHLH subunit might play an important regulatory role when the chlorophyll biosynthetic pathway is disrupted at this particular step

Parasite-Parasite Interactions in the Wild: How To Detect Them?

International audienceInter-specific interactions between parasites impact on parasite intra-hostdynamics, host health, and disease management. Identifying and understandinginteraction mechanisms in the wild is crucial for wildlife disease management.It is however complex because several scales are interlaced. Parasite–parasite interactions are likely to occur via mechanisms at the within-host level,but also at upper levels (host population and community). Furthermore, interactionsoccurring at one level of organization spread to upper levels throughcascade effects. Even if cascade effects are important confounding factors, weargue that we can also benefit from them because upper scales often provide away to survey a wider range of parasites at lower cost. New protocols andtheoretical studies (especially across scales) are necessary to take advantage ofthis opportunity

Evolution of microparasites in spatially and genetically structured host populations: The example of RHDV infecting rabbits

International audienc

The m 6 A pathway protects the transcriptome integrity by restricting RNA chimera formation in plants

International audienceGlobal, segmental, and gene duplication-related processes are driving genome size and complexity in plants. Despite their evolutionary potentials, those processes can also have adverse effects on genome regulation, thus implying the existence of specialized corrective mechanisms. Here, we report that an N6-methyladenosine (m 6 A)-assisted polyadenylation (m-ASP) pathway ensures tran-scriptome integrity in Arabidopsis thaliana. Efficient m-ASP pathway activity requires the m 6 A methyltransferase-associated factor FIP37 and CPSF30L, an m 6 A reader corresponding to an YT512-B Homology Domain-containing protein (YTHDC)-type domain containing isoform of the 30-kD subunit of cleavage and polyadenylation specificity factor. Targets of the m-ASP pathway are enriched in recently rearranged gene pairs, displayed an atypical chromatin signature, and showed transcriptional readthrough and mRNA chimera formation in FIP37-and CPSF30L-deficient plants. Furthermore, we showed that the m-ASP pathway can also restrict the formation of chimeric gene/transposable-element transcript, suggesting a possible implication of this pathway in the control of transposable elements at specific locus. Taken together, our results point to selective recognition of 39-UTR m 6 A as a safeguard mechanism ensuring transcriptome integrity at rearranged genomic loci in plants

Complete Genome and Phylogeny of Puumala Hantavirus Isolates Circulating in France

Puumala virus (PUUV) is the agent of nephropathia epidemica (NE), a mild form of hemorrhagic fever with renal syndrome (HFRS) in Europe. NE incidence presents a high spatial variation throughout France, while the geographical distribution of the wild reservoir of PUUV, the bank vole, is rather continuous. A missing piece of the puzzle is the current distribution and the genetic variation of PUUV in France, which has been overlooked until now and remains poorly understood. During a population survey, from 2008 to 2011, bank voles were trapped in eight different forests of France located in areas known to be endemic for NE or in area from where no NE case has been reported until now. Bank voles were tested for immunoglobulin (Ig)G ELISA serology and two seropositive animals for each of three different areas (Ardennes, Jura and Orleans) were then subjected to laboratory analyses in order to sequence the whole S, M and L segments of PUUV. Phylogenetic analyses revealed that French PUUV isolates globally belong to the central European (CE) lineage although isolates from Ardennes are clearly distinct from those in Jura and Orleans, suggesting a different evolutionary history and origin of PUUV introduction in France. Sequence analyses revealed specific amino acid signatures along the N protein, including in PUUV from the Orleans region from where NE in humans has never been reported. The relevance of these mutations in term of pathophysiology is discussed.Peer reviewe

Genome-wide computational identification of WG/GW Argonaute-binding proteins in Arabidopsis

Domains in Arabidopsis proteins NRPE1 and SPT5-like, composed almost exclusively of repeated motifs in which only WG or GW sequences and an overall amino-acid preference are conserved, have been experimentally shown to bind multiple molecules of Argonaute (AGO) protein(s). Domain swapping between the WG/GW domains of NRPE1 and the human protein GW182 showed a conserved function. As classical sequence alignment methods are poorly-adapted to detect such weakly-conserved motifs, we have developed a tool to carry out a systematic analysis to identify genes potentially encoding AGO-binding GW/WG proteins. Here, we describe exhaustive analysis of the Arabidopsis genome for all regions potentially encoding proteins bearing WG/GW motifs and consider the possible role of some of them in AGO-dependent mechanisms. We identified 20 different candidate WG/GW genes, encoding proteins in which the predicted domains range from 92aa to 654aa. These mostly correspond to a limited number of families: RNA-binding proteins, transcription factors, glycine-rich proteins, translation initiation factors and known silencing-associated proteins such as SDE3. Recent studies have argued that the interaction between WG/GW-rich domains and AGO proteins is evolutionarily conserved. Here, we demonstrate by an in silico domain-swapping simulation between plant and mammalian WG/GW proteins that the biased amino-acid composition of the AGO-binding sites is conserved