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F-actin nanostructures rearrangements and regulation are essential for SARS-CoV-2 particle production in host pulmonary cells

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Rubio,  Karla
Lung Cancer Epigenetics, Max Planck Institute for Heart and Lung Research, Max Planck Society;

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Guenther,  Stefan
Cardiac Development and Remodeling, Max Planck Institute for Heart and Lung Research, Max Planck Society;

/persons/resource/persons224344

Barreto,  Guillermo
Lung Cancer Epigenetics, Max Planck Institute for Heart and Lung Research, Max Planck Society;

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Citation

Swain, J., Merida, P., Rubio, K., Bracquemond, D., Neyret, A., Aguilar-Ordon, I., et al. (2023). F-actin nanostructures rearrangements and regulation are essential for SARS-CoV-2 particle production in host pulmonary cells. ISCIENCE, 26(8): 107384. doi:10.1016/j.isci.2023.107384.


Cite as: https://hdl.handle.net/21.11116/0000-000D-AFEC-5
Abstract
Our study focused on deciphering the role of F-actin and related regulatory factors during SARS-CoV-2 particle production and transmission in human pulmonary cells. Quantitative high-resolution microscopies revealed that the late phases of SARS-CoV-2 infection induce a strong rearrangement of F-actin nanostructures dependent on the viral M, E, and N structural proteins. Intracel-lular vesicles containing viral components are labeled with Rab7 and Lamp1 and are surrounded by F-actin ring-shaped structures, suggesting their role in viral trafficking toward the cell membrane for virus release. Furthermore, filopo-dia-like nanostructures were loaded with viruses, potentially facilitating their egress and transmission between lung cells. Gene expression analysis revealed the involvement of alpha-actinins under the regulation of the protein kinase N (PKN). The use of a PKN inhibitor efficiently reduces virus particle production, restoring endoplasmic reticulum and F-actin cellular shape. Our results highlight an important role of F-actin rearrangements during the productive phases of SARS-CoV-2