Intracontinental deformation in southern Africa during the late Cretaceous

Intracontinental deformation accommodated along major lithospheric scale shear zone systems and within associated extensional basins has been well documented within West, Central and East Africa during the Late Cretaceous. The nature of this deformation has been established by studies of the tectonic architecture of sedimentary basins preserved in this part of Africa. In southern Africa, where the post break-up history has been dominated by major erosion, little evidence for post-break-up tectonics has been preserved in the onshore geology. Here we present the results of 38 new apatite fission track analyses from the Damara region of northern Namibia and integrate these new data with our previous results that were focused on specific regions or sections only to comprehensively document the thermo-tectonic history of this region since continental break-up in the Early Cretaceous. The apatite fission track ages range from 449 ± 20 Ma to 59 ± 3 Ma, with mean confined track lengths between 14.61 ± 0.1 μm (SD 0.95 μm) to 10.83 ± 0.33 μm (SD 2.84 μm). The youngest ages (c. 80-60 Ma) yield the shortest mean track lengths, and combined with their spatial distribution, indicate major cooling during the latest Cretaceous. A simple numerical thermal model is used to demonstrate that this cooling is consistent with the combined effects of heating caused by magmatic underplating, related to the Etendeka continental flood volcanism associated with rifting and the opening of the South Atlantic, and enhanced erosion caused by major reactivation of major lithospheric structures within southern Africa during a key period of plate kinematic change that occurred in the South Atlantic and SW Indian ocean basins between 87-56 Ma. This phase of intraplate tectonism in northern Namibia, focused in discrete structurally defined zones, is coeval with similar phases elsewhere in Africa and suggests some form of trans-continental linkage between these lithospheric zones

Ontogenetic Shifts in the Costs of Living in Groups: Focal Observations of a Pholcid Spider (Holocnemus pluchei)

Holocnemus pluchei spiders (Family Pholcidae) facultatively live in groups: sometimes they live alone and sometimes they share webs. In the field groups vary in size and composition and include spiders of all ages and either sex. Group membership is flexible and individuals move frequently among groups. To understand group formation and maintenance it is necessary to understand the costs of group membership. We used focal animal sampling to investigate the cost of group living for spiders of different ages across a range of group sizes. Both spider age and group size affected the costs incurred by group-living spiders. There was no variation among groups of different sizes in the percentage of time focal small or large spiders spent in costly behaviors (moving, web maintenance, bouncing or interactions with conspecifics), but medium-sized spiders spent more time engaged in costly behaviors with increasing group size. Medium and large spiders also had more interactions with greater numbers of different conspecifics when they were in groups larger than three, whereas small spiders interacted rarely with conspecifics regardless of group size. These results suggest that there are significant ontogenetic shifts in the costs of group living in H. pluchei

Impact of genotype 1 and 2 of porcine reproductive and respiratory syndrome viruses on interferon-α responses by plasmacytoid dendritic cells

Porcine reproductive and respiratory syndrome (PRRS) virus (PRRSV) infections are characterized by prolonged viremia and viral shedding consistent with incomplete immunity. Type I interferons (IFN) are essential for mounting efficient antiviral innate and adaptive immune responses, but in a recent study, North American PRRSV genotype 2 isolates did not induce, or even strongly inhibited, IFN-α in plasmacytoid dendritic cells (pDC), representing "professional IFN-α-producing cells". Since inhibition of IFN-α expression might initiate PRRSV pathogenesis, we further characterized PRRSV effects and host modifying factors on IFN-α responses of pDC. Surprisingly, a variety of type 1 and type 2 PRRSV directly stimulated IFN-α secretion by pDC. The effect did not require live virus and was mediated through the TLR7 pathway. Furthermore, both IFN-γ and IL-4 significantly enhanced the pDC production of IFN-α in response to PRRSV exposure. PRRSV inhibition of IFN-α responses from enriched pDC stimulated by CpG oligodeoxynucleotides was weak or absent. VR-2332, the prototype genotype 2 PRRSV, only suppressed the responses by 34%, and the highest level of suppression (51%) was induced by a Chinese highly pathogenic PRRSV isolate. Taken together, these findings demonstrate that pDC respond to PRRSV and suggest that suppressive activities on pDC, if any, are moderate and strain-dependent. Thus, pDC may be a source of systemic IFN-α responses reported in PRRSV-infected animals, further contributing to the puzzling immunopathogenesis of PRRS

Interactions of human microglia cells with Japanese encephalitis virus

Japanese encephalitis virus (JEV) is a neurotropic flavivirus causing mortality and morbidity in humans. Severe Japanese encephalitis cases display strong inflammatory responses in the central nervous system and an accumulation of viral particles in specific brain regions. Microglia cells are the unique brain-resident immune cell population with potent migratory functions and have been proposed to act as a viral reservoir for JEV. Animal models suggest that the targeting of microglia by JEV is partially responsible for inflammatory reactions in the brain. Nevertheless, the interactions between human microglia and JEV are poorly documented.Methods: Using human primary microglia and a new model of human blood monocyte-derived microglia, the present study explores the interaction between human microglia and JEV as well as the role of these cells in viral transmission to susceptible cells. To achieve this work, vaccine-containing inactivated JEV and two live JEV strains were applied on human microglia.Results: Live JEV was non-cytopathogenic to human microglia but increased levels of CCL2, CXCL9 and CXCL10 in such cultures. Furthermore, human microglia up-regulated the expression of the fraktalkine receptor CX3CR1 upon exposure to both JEV vaccine and live JEV. Although JEV vaccine enhanced MHC class II on all microglia, live JEV enhanced MHC class II mainly on CX3CR1+ microglia cells. Importantly, human microglia supported JEV replication, but infectivity was only transmitted to neighbouring cells in a contact-dependent manner.Conclusion: Our findings suggest that human microglia may be a source of neuronal infection and sustain JEV brain pathogenesis

Interactions of human microglia cells with Japanese encephalitis virus

Japanese encephalitis virus (JEV) is a neurotropic flavivirus causing mortality and morbidity in humans. Severe Japanese encephalitis cases display strong inflammatory responses in the central nervous system and an accumulation of viral particles in specific brain regions. Microglia cells are the unique brain-resident immune cell population with potent migratory functions and have been proposed to act as a viral reservoir for JEV. Animal models suggest that the targeting of microglia by JEV is partially responsible for inflammatory reactions in the brain. Nevertheless, the interactions between human microglia and JEV are poorly documented.Methods: Using human primary microglia and a new model of human blood monocyte-derived microglia, the present study explores the interaction between human microglia and JEV as well as the role of these cells in viral transmission to susceptible cells. To achieve this work, vaccine-containing inactivated JEV and two live JEV strains were applied on human microglia.Results: Live JEV was non-cytopathogenic to human microglia but increased levels of CCL2, CXCL9 and CXCL10 in such cultures. Furthermore, human microglia up-regulated the expression of the fraktalkine receptor CX3CR1 upon exposure to both JEV vaccine and live JEV. Although JEV vaccine enhanced MHC class II on all microglia, live JEV enhanced MHC class II mainly on CX3CR1+ microglia cells. Importantly, human microglia supported JEV replication, but infectivity was only transmitted to neighbouring cells in a contact-dependent manner.Conclusion: Our findings suggest that human microglia may be a source of neuronal infection and sustain JEV brain pathogenesis

Efficient Sensing of Avian Influenza Viruses by Porcine Plasmacytoid Dendritic Cells

H5N1 influenza A virus (IAV) infections in human remain rare events but have been associated with severe disease and a higher mortality rate compared to infections with seasonal strains. An excessive release of pro-inflammatory cytokine together with a greater virus dissemination potential have been proposed to explain the high virulence observed in human and other mammalian and avian species. Among the cells involved in the cytokine storm, plasmacytoid dendritic cells (pDC) could play an important role considering their unique capacity to secrete massive amounts of type I interferon (IFN). Considering the role of IFN as a major component of antiviral responses as well as in priming inflammatory responses, we aimed to characterize the induction of IFN-α release upon infection with IAV originating from various avian and mammalian species in a comparative way. In our porcine pDC model, we showed that the viral components triggering IFN responses related to the ability to hemagglutinate, although virosomes devoid of viral RNA were non-stimulatory. Heat-treatment at 65 °C but not chemical inactivation destroyed the ability of IAV to stimulate pDC. All IAV tested induced IFN-α but at different levels and showed different dose-dependencies. H5 and H7 subtypes, in particular H5N1, stimulated pDC at lower doses when compared to mammalian IAV. At high viral doses, IFN-α levels reached by some mammalian IAV surpassed those induced by avian isolates. Although sialic acid-dependent entry was demonstrated, the α-2,3 or α-2,6 binding specificity alone did not explain the differences observed. Furthermore, we were unable to identify a clear role of the hemagglutinin, as the IFN-α doses-response profiles did not clearly differ when viruses with all genes of identical avian origin but different HA were compared. This was found with IAV bearing an HA derived from either a low, a high pathogenic H5N1, or a human H3. Stimulation of pDC was associated with pDC depletion within the cultures. Taken together and considering the efficient sensing of H5N1 at low dose, pDC on one side may play a role in the cytokine storm observed during severe disease, on the other hand could participate in early antiviral responses limiting virus replication