The multistage crystallization of zircon in calc-alkaline granitoids: U–Pb age constraints on the timing of Variscan tectonic activity in SW Iberia

CL imaging and U–Th–Pb data for a population of zircons from two of the Évora Massif granitoids(Ossa-Morena Zone, SW Iberia) show that both calcalkaline granitoids have zircon populations dominated by grains with cores and rims either showing or not showing differences in Th/U ratio, and having ages in the range ca. 350–335 Ma (Early Carboniferous). Multistage crystallization of zircon is revealed in two main growth stages(ca. 344–342 Ma and ca. 336–335 Ma), well represented by morphologically complex zircons with cores and rims with different ages and different Th/U ratios that can be explained by: (1) crystallization from melts with different compositions (felsic peraluminous to felsic-intermediate metaluminous; 0.001 837 °C; granulite facies)and/or because they were derived from inheritance-poor felsic and mafic rocks from a previous cycle, as suggested by the internal structures of zircon cores. These Variscan magmatic rocks with crystallization ages estimated at ca. 336–335 Ma are spatially and temporally related to hightemperature metamorphism, anatexis, processes of interaction between crustal- and mantle derived magmas and intra-orogenic extension that acted in SW Iberia during the Early Carboniferous

Subversion of the B-cell compartment during parasitic, bacterial, and viral infections

International audienceAbstractRecent studies on HIV infection have identified new human B-cell subsets with a potentially important impact on anti-viral immunity. Current work highlights the occurrence of similar B-cell alterations in other viral, bacterial, and parasitic infections, suggesting that common strategies have been developed by pathogens to counteract protective immunity. For this review, we have selected key examples of human infections for which B-cell alterations have been described, to highlight the similarities and differences in the immune responses to a variety of pathogens. We believe that further comparisons between these models will lead to critical progress in the understanding of B-cell mechanisms and will open new target avenues for therapeutic interventions