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. 2020 Nov 19;3:688. doi: 10.1038/s42003-020-01422-1

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 7 — The data supports the model that C4 overcomes the protective function of UIS3 during Plasmodium intrahepatic development. In the presence of C4, UIS3 cannot sequester LC3 rendering the downstream autophagy receptors to interact with it. As a result, the host autophagy pathway remains active leading to the lysosome fusion with the PVM and elimination of the parasite from the hepatocyte.