Search

International audience; Emerging infectious diseases can induce rapid changes in population dynamics and threaten population persistence. In socially structured populations, the transfers of individuals between social units, for example, from breeding groups to non-breeding groups, shape population dynamics. We suggest that diseases may affect these crucial transfers. We aimed to determine how disturbance by an emerging disease affects demographic rates of gorillas, especially transfer rates within populations and immigration rates into populations. We compared social dynamics and key demographic parameters in a gorilla population affected by Ebola using a long-term observation data set including pre-, during and post-outbreak periods. We also studied a population of undetermined epidemiological status in order to assess whether this population was affected by the disease. We developed a multistate model that can handle transition between social units while optimizing the number of states. During the Ebola outbreak, social dynamics displayed increased transfers from a breeding to a non-breeding status for both males and females. Six years after the outbreak, demographic and most of social dynamics parameters had returned to their initial rates, suggesting a certain resilience in the response to disruption. The formation of breeding groups increased just after Ebola, indicating that environmental conditions were still attractive. However, population recovery was likely delayed because compensatory immigration was probably impeded by the potential impact of Ebola in the surrounding areas. The population of undetermined epidemiological status behaved similarly to the other population before Ebola. Our results highlight the need to integrate social dynamics in host-population demographic models to better understand the role of social structure in the sensitivity and the response to disease disturbances.

12 pages; International audience; Invasive species may introduce novel pathogens to a colonised area. Most of the time emerging pathogens are detected a posteriori, but recognition of a priori emergence of an invasive disease by host shift may be useful for predictive purposes. Here, we studied if the microsporidian parasite Cucumispora dikerogammari infecting the invasive Ponto-Caspian amphipod Dikerogammarus villosus, has the potential to become an emergent disease in invaded rivers in Western and Central Europe. We first showed that this parasite decreases the survival of D. villosus in the later stages of infection development. However, the host reproduces earlier in response to the infection, which could potentially reduce the negative impact of the parasite on host populations. Cucumispora dikerogammari is able to infect other crustacean species as revealed by our experimental infections. However, field census showed that it was found in other Ponto-Caspian species of amphipods only when it was observed in high prevalence in its native host, and when this host was at moderate frequencies in the community. Therefore, adaptation of C. dikerogammari to native gammaridean hosts has probably not been realized in the wild yet. However, since several environmental factors may promote future adaptations of the parasite to novel host species, we suggest C. dikerogammari should be included in surveillance networks for emergent disease in freshwater.

International audience; Plasma cells represent the end stage of B-cell development and play a key role in providing an efficient antibody response, but they are also involved in numerous pathologies. Here we show that CD93, a receptor expressed during early B-cell development, is reinduced during plasma-cell differentiation. High CD93/CD138 expression was restricted to antibody-secreting cells both in T-dependent and T-independent responses as naive, memory, and germinal-center B cells remained CD93-negative. CD93 was expressed on (pre)plasmablasts/plasma cells, including long-lived plasma cells that showed decreased cell cycle activity, high levels of isotype-switched Ig secretion, and modification of the transcriptional network. T-independent and T-dependent stimuli led to re-expression of CD93 via 2 pathways, either before or after CD138 or Blimp-1 expression. Strikingly, while humoral immune responses initially proceeded normally, CD93-deficient mice were unable to maintain antibody secretion and bone-marrow plasma-cell numbers, demonstrating that CD93 is important for the maintenance of plasma cells in bone marrow niches.