Figures
Plasmodium parasites recruit host aquaporin-3 for proper development
When Plasmodium parasites are injected into the bloodstream via the bite of a mosquito, they first travel to the liver where they undergo morphological changes and rapid asexual replication before invading red blood cells and cause disease. The parasites rely on the host liver environment to undergo these changes. Immunofluorescence image of Plasmodium-infected hepatocytes show host aquaporin-3 (red) is recruited to the parasitophorous vacuole membrane of the parasites (nuclei, blue) within hepatocytes (nuclei, white). Disruption of host aquaporin-3 prevents proper parasite development. Derbyshire et al.
Image Credit: Dora Posfai and Emily Derbyshire, Duke University
Citation: (2018) PLoS Pathogens Issue Image | Vol. 14(5) May 2018. PLoS Pathog 14(5): ev14.i05. https://doi.org/10.1371/image.ppat.v14.i05
Published: May 31, 2018
Copyright: © 2018 Posfai and Derbyshire, Duke University. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
When Plasmodium parasites are injected into the bloodstream via the bite of a mosquito, they first travel to the liver where they undergo morphological changes and rapid asexual replication before invading red blood cells and cause disease. The parasites rely on the host liver environment to undergo these changes. Immunofluorescence image of Plasmodium-infected hepatocytes show host aquaporin-3 (red) is recruited to the parasitophorous vacuole membrane of the parasites (nuclei, blue) within hepatocytes (nuclei, white). Disruption of host aquaporin-3 prevents proper parasite development. Derbyshire et al.
Image Credit: Dora Posfai and Emily Derbyshire, Duke University