Researchers from the Membramics Lab, in collaboration with teams at Institut Pasteur and the Institute of Psychiatry and Neuroscience of Paris, have uncovered a novel mechanism by which Influenza A virus (IAV) manipulates host cell membranes to ensure the export of its genome.

The study, led by Carla Alemany and Juliane Da Graça (equal contribution), shows that IAV infection leads to reorganization of endoplasmic reticulum (ER) membranes and a local increase in phosphatidylinositol-4-phosphate (PI4P) levels. This remodeling relies on the autophagy-related protein ATG16L1, which relocates to ER membranes during infection.

Depletion of ATG16L1 prevents the proper accumulation of viral ribonucleoproteins (vRNPs) at PI4P-enriched ER sites, impairs their delivery to the plasma membrane, and reduces viral particle production.

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These findings identify the ER as a key platform for coordinating lipid signaling and membrane identity during viral egress, and highlight the role of proteins of the autophagy machinery in regulating intracellular trafficking and the hijacking of this function by pathogens.

Read the article: https://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.3002958#abstract0