Periodontitis is one of the most common human inflammatory condition. This disease is responsible for tooth mobility and tooth loss, and it is also a significant risk factor for dozens of seemingly unrelated systemic illnesses. A polymicrobial dysbiosis model was proposed for periodontitis with colonization of subgingival teeth sites with different Gram-negative bacteria, identified as “keystone pathogens”.

So far, most studies have focused on bacterial populations, while less attention has been paid to the viral component. We notably investigated the pathogenic role of the Epstein-Barr virus in periodontitis showing that the virus can promote breakdown of innate barriers, pro-inflammatory signaling, and immune dysregulation and thus deeply worsening severity of the disease

We wish to uncover the rules governing gene expression in response to developmental and extra-cellular cues. Genome architecture is thought to be a major determinant in this. What we strive to understand is how chromatin (re)folds to accommodate responses to such cues in 3D nuclear space and dynamically over time. In the end, we anticipate these rules to be general ones, which once deciphered will allow us to predict how a cell might respond upon signalling, in the context of disease, or during cellular ageing.