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. 2016 Jul 7;6:28694. doi: 10.1038/srep28694

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Copyright © 2016, Macmillan Publishers Limited

This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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Based on the data from this study, CME, macropinocytosis and caveolae-mediated endocytosis are clearly employed for both WSSV entry and viral replication in Hpt cell. Cq-GABARAP, a key autophagy-related molecule that can bind to both WSSV and cytoskeleton components, is co-localized with the viral envelope protein VP28 on the cell membrane, leading to the promoted WSSV entry possibly by 1) binding to WSSV virions; 2) cooperating with cytoskeletal proteins such as β-actin and β-tubulin; 3) enhancing CME activity via suppression of the Rac1 signaling pathway; 4) increasing autophagic activity. However, WSSV replication is suppressed in the presence of rCq-GABARAP after its entry into Hpt cell, which may be attributed to the intracellular formation of WSSV aggregates that delay transport of virions from the cytoplasm into the nucleus for successful replication.