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Ruelle, J.

Publications and source records attributed to Ruelle, J..

2 recordsLinked to original sources

Nest aggregations of wild bees and apoid wasps in urban pavements: a street life to be promoted in urban planning

In the last 10 years, knowledges of wild bees and apoid wasps community dynamics have gained interest in urban ecology focusing on the availability of floral resources in cities. Although understudied, the urban environment impacts the conditions of their nesting sites. Recent observations in the Brussels-Capital Region (Belgium) showed that urban pavements can be a novel nesting opportunity for Hymenoptera ground-nesting species such as wild bees and apoid wasps. Here, using citizen science, we investigated the richness of ground-nesting species living under urban pavements, the preferences of the sidewalk joint size related to ground-nesting species size and for sidewalk type or for soils texture under the pavements on the nesting site selection. A total of 22 species belonging to 10 Hymenoptera families of wild bees and digger wasps with their associated kleptoparasites were identified on 89 sites in Brussels. Sandstone setts or concrete slabs with an unbound joint size around 1 cm were found to be best suitable urban pavements for the ground-nesting species. The soil texture under the pavement was highly sandy among our samples. Finally, we also suggest engineering management guidelines to support bee and wasp species nesting under urban pavement in highly urbanized areas. Such observations pave the way for much research in the field of urban ecology to conceive multifunctional pavement promoting biodiversity.

ecology↗

HIV-1 and HIV-2 differentially regulate NF-κB activity during the late stages of the replication cycle through BST-2/tetherin antagonism

HIV-2 is the second causative agent of AIDS and is commonly considered as an attenuated form of retroviral infection. Most of HIV-2-infected individuals display a slow-progressing disease, lower viral loads and a stronger immunological control of viral infection as compared with HIV-1-infected patients. The main hypothesis that could explain the difference of disease progression between HIV-1 and HIV-2 implies a more efficient T cell-mediated immunity in the control of HIV-2 infection. Herein, we investigate the effects of the HIV-2 envelope glycoprotein (Env) and its antitetherin function in the NF-{kappa}B signaling pathway during single-round infection of CD4+ T cells. First, we report an essential role of the Env cytoplasmic tail (CT) in the activation of this signaling pathway and we also demonstrate that the HIV-2 Env CT activates NF-{kappa}B in a TRAF6-dependent but TAK1-independent manner. Further, we show that HIV-2 reference strains and clinical isolates are unable to completely inhibit NF-{kappa}B mainly via the Env-mediated BST-2/tetherin antagonism in the late stages of the viral replication cycle in CD4+ T cells, in striking contrast to the HIV-1 Vpu-mediated counteraction of tetherin. We observe that this inability of HIV-2 to suppress NF-{kappa}B signaling pathway promotes stimulation of numerous genes involved in the antiviral immune response, such as il-6, il-21 and ifn-{beta} genes. Therefore, HIV-1 and HIV-2 differentially regulate the NF-{kappa}B-induced antiviral immune response mainly through the BST-2/tetherin antagonism. These new insights highlight molecular mechanisms determining, at least partly, the distinct immune control and disease outcomes of HIV-1 and HIV-2 infections. IMPORTANCEThis study explores how HIV-1 and HIV-2 diverge in their regulation of the NF-{kappa}B signaling pathway. We revealed that HIV-2 fails to completely inhibit NF-{kappa}B activity, thereby inducing a stronger antiviral response than HIV-1. We demonstrated that the ability to antagonize the cellular restriction factor BST-2/tetherin largely governs the regulation of the NF-{kappa}B pathway: at the late stages of the viral replication cycle, HIV-1 Vpu blocks this pathway whereas HIV-2 Env does not. We also demonstrated that several NF-{kappa}B-targeted genes are upregulated in CD4+ T cells infected with HIV-2, but not with HIV-1. This stronger NF-{kappa}B-induced antiviral response may explain the better immune control of HIV-2 infection and the differences between HIV-1 and HIV-2 pathogenesis. Moreover, we observed in this study that non-pathogenic isolates of HIV-2 have an impaired NF-{kappa}B inhibitory capacity compared to pathogenic ones.

microbiology↗