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
Opinion
Does pathogen plasticity facilitate host shifts?
PLOS Pathogens: published May 3, 2018 | https://doi.org/10.1371/journal.ppat.1006961
Pearls
RNA virus building blocks—miRNAs not included
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