Link to bioRxiv paper:
http://biorxiv.org/cgi/content/short/2023.02.04.527154v1?rss=1

Authors: Liu, W., Lu, J.-Y., Wang, Y.-J., Xu, X.-x., Chen, Y.-C., Yu, S.-X., Xiang, X.-W., Chen, X.-Z., Jiu, Y., Gao, H., Sheng, M., Chen, Z.-J., Hu, X., Li, D., Maiuri, P., Huang, X., Ying, T., Xu, G.-L., Pang, D.-W., Zhang, Z.-L., Liu, B., Liu, Y.-J.

Abstract:
The emerging outbreak of monkeypox is closely associated with the viral infection and spreading, threatening global public health. Virus-induced cell migration facilitates viral transmission. However, high-resolution dynamics and mechanisms underlying this type of cell migration remain unclear. Here, we investigate the motility of cells infected by vaccinia virus (VACV), a close relative of monkeypox, through combining multi-omics analyses and high-resolution live-cell imaging. We find that, upon VACV infection, the epithelial cells undergo EMT-like transformation, during which they lose intercellular junctions and acquire the migratory capacity to promote viral spreading. After transformation, VACV-induced mesenchymal migration is highly dependent on the actin cytoskeleton and RhoA signaling, which is responsible for the depolymerization of robust actin stress fibers, the leading-edge protrusion formation, and the rear-edge recontraction. Our study reveals how poxviruses alter the epithelial phenotype and regulate RhoA signaling to induce fast migration, providing a unique perspective to understand the pathogenesis of poxviruses.

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