Dear all,
We are pleased to welcome Harald WODRICH from the Microbiologie Fondamentale et Pathogénicité (MFP) institute in Bordeaux, invited by Patrick LOMONTE
He will give a seminar on June, 11th at 11:00 a.m. entitled: “Where Infection Begins: Endosomal Escape as Determinant of Viral success”
The seminar will take place in Amphi 3 (3rd floor).
Harald Wodrich is Research Director (INSERM DR2) and group leader at the Microbiologie Fondamentale et Pathogénicité (MFP) institute, CNRS/University of Bordeaux, where he leads the team “Spatial and Temporal Control of Virus–Host Interactions.”
His research focuses on the cell biology of DNA viruses, in particular adenoviruses, with an emphasis on how viral particles deliver their genomes into host cells and evade cellular defenses. His work has uncovered key mechanisms of viral entry, including membrane disruption by capsid protein VI and viral modulation of antiviral autophagy, and has contributed to understanding how incoming viral genomes are trafficked, imported into the nucleus, and converted into transcriptionally active templates.
A central aspect of his research is the development of advanced imaging approaches to visualize viral particles, individual viral genomes and virus–host interactions at high spatial and temporal resolution.
Harald Wodrich obtained his PhD from the University of Hamburg and conducted postdoctoral research at the Scripps Research Institute (USA) before establishing his group in France. He has authored over 70 publications and is actively involved in international collaborations and scientific evaluation panels.
Abstract
Adenoviruses enter cells by receptor-mediated endocytosis. As non-enveloped DNA viruses, they must escape the endosomal compartment to reach the nucleus for replication. This creates a fundamental conundrum: damaging the endosomal membrane alerts the cell and triggers multiple defense pathways.
We show that incoming viral particles are not passive carriers but actively engage these host pathways during entry. In particular, the site and timing of endosomal escape emerge as key determinants of infection outcome, influencing exposure to innate immune sensors and antiviral processes such as autophagy. Viral structural proteins play a dual role in this process, both protecting the genome and modulating host responses to promote productive infection.
In this presentation, I will highlight how adenoviruses are optimized to control cellular responses, providing insight into viral pathogenicity and informing the design of improved gene delivery vectors.
References
TBK1 is part of a galectin 8 dependent membrane damage recognition complex and drives autophagy upon Adenovirus endosomal escape. Pied N, Daussy CF, Denis Z, Ragues J, Faure M, Iggo R, Tschan MP, Roger B, Rayne F, Wodrich H. PLoS Pathog. 2022
Multi-layered control of Galectin-8 mediated autophagy during adenovirus cell entry through a conserved PPxY motif in the viral capsid. Montespan C, Marvin SA, Austin S, Burrage AM, Roger B, Rayne F, Faure M, Campell EM, Schneider C, Reimer R, Grünewald K, Wiethoff CM, Wodrich H. PLoS Pathog. 2017
Understanding Post Entry Sorting of Adenovirus Capsids; A Chance to Change Vaccine Vector Properties. Daussy CF, Pied N, Wodrich H. Viruses. 2021
« Repair Me if You Can »: Membrane Damage, Response, and Control from the Viral Perspective. Daussy CF, Wodrich H. Cells. 2020