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Bellucci, G.

Publications and source records attributed to Bellucci, G..

3 recordsLinked to original sources

Enrichment analysis of GWAS data in autoimmunity delineates the multiple sclerosis-Epstein Barr virus association

We exploited genetic information to assess non-genetic influences in autoimmunity. We isolated gene modules whose products physically interact with environmental exposures related to autoimmunity, and analyzed their nominal statistical evidence of association with autoimmune and non-autoimmune diseases in genome-wide association studies (GWAS) data. Epstein Barr virus (EBV) and other Herpesviruses interactomes emerged as specifically associated with multiple sclerosis (MS), possibly under common regulatory mechanisms. Analyses of MS blood and brain transcriptomes, cytofluorimetric studies of endogenous EBV-infected lymphoblastoid lines, and lesion immunohistochemistry, confirmed a dysregulation of MS-associated EBV interactors, suggesting their contribution to CD40 signaling alterations in MS. These interactors resulted enriched in modules from inherited axonopathies-causing genes, supporting a link between EBV and neurodegeneration in MS, in accord with the observed transcriptomic dysregulations in MS brains. They were also enriched with top-ranked pharmaceutical targets prioritized on a genetic basis. This study delineates a disease-specific influence of herpesviruses on MS biology.

neuroscience

GWAS-associated variants, non-genetic factors and transient transcriptome in Multiple Sclerosis etiopathogenesis: a colocalization analysis

A clinically actionable understanding of multiple sclerosis (MS) etiology goes through GWAS interpretation, prompting research on new gene regulatory models. We previously suggested a stochastic etiologic model where small-scale random perturbations could reach a threshold for MS development. The recently described mapping of the transient transcriptome (TT), including intergenic and intronic RNAs, seems appropriate to verify this model through a rigorous colocalization analysis. We show that genomic regions coding for the TT were significantly enriched for MS-associated GWAS variants and DNA binding sites for molecular transducers mediating putative, non-genetic, etiopathogenetic factors for MS (e.g., vitamin D deficiency, Epstein Barr virus latent infection, B cell dysfunction). These results suggest a model whereby TT-coding regions are hotspots of convergence between genetic ad non-genetic factors of risk/protection for MS, and plausibly for other complex disorders. Our colocalization analysis also provides a freely available data resource (www.mscoloc.com) for future research on MS transcriptional regulation.

neuroscience

Demographics and Employment of Max-Planck Society's Postdocs

The recently founded Max Planck PostdocNet brings together postdoctoral researchers (or postdocs) from the Max Planck Society (MPS), provides representation for the postdoctoral community across all Max Planck Institutes (MPI) and associated institutes, and advocates for their interests on their behalf. At the 2019 founding meeting, MPS postdocs quickly raised their concerns about their employment situation and their associated social and working conditions. Subsequently, the PostdocNet conducted the first survey targeting exclusively postdoctoral researchers to gather information on their demographics, employment situations and social conditions. This report presents the results of this survey, providing a thorough characterization of the postdoc demographics as well as the working conditions experienced by the postdoctoral community of the MPS. Remarkably, the survey analysis revealed a number of disparities in the access to employment type, wage level and social benefits. These results will guide future and present MPS postdoctoral researchers and their employers at the MPS to thrive for equality and fairness. Moreover, these results should be of help to the MPS to establish, improve and maintain optimal working conditions for MPS postdocs.

scientific communication and education