Parasite plasma membrane

Since a malaria-infected red cell contains three membrane interfaces the plasma membrane of the red cell, the parasitophorous vacuolar membrane (PVM) and the parasite plasma membrane (PPM) studying membrane transport in such a system is not straightforward. Substrates have to traverse multiple membrane systems and a single membrane may contain multiple transporters for a particular substrate. To complicate the matter further, when we (and others) embarked on such studies not only were we usually unaware of the complexities of the transport systems that might be encountered, we were also unappreciative of the technical difficulties as well as possible artefacts that might result from isolating parasites and using heavy infections in unnatural hosts or from in vitro cultures. 

Downie, M. J., Saliba, K. J., Howitt, S. M., Broer, S., and Kirk, K. (2006). Transport of nucleosides across the Plasmodium falciparum parasite plasma membrane has characteristics of PfENTl. Mol. Microbiol. 60, 738-748. 

Rager, N., Mamoun, C. B., Carter, N. S., Goldberg, D. E., and Ullman, B. (2001). Localization of the Plasmodium falciparum PfNTl nucleoside transporter to the parasite plasma membrane.. Biol. Chem. 276,41095-41099. 

The antigens on these parasites stimulate B-cells to produce IgE antibodies which do two things (i) they coat (opsoifise) the parasite and (ii) they bind to the mast cell via a specific receptor. The parasite is sufficiently large that many eosinophils bind to it, via the IgE antibodies. Many of the eosinophils are so close that they are in direct contact with the plasma membrane of the parasite. The lysosome of the eosinophil can fuse with the plasma membrane and the contents of the lysosome are released in close proximity to the parasite, which is then damaged or killed by proteolytic and other enzymes (Figure 17.34). 

Viruses (from the Latin virus referring to poison) are nonliving obligate intracellular parasites composed of protein and nucleic acid (DNA or RNA) that manipulate the host cell to produce and manufacture more viruses. Viral infection occurs by tire attachment of virus particles to specific cell receptors within the host cell. After fusion of the host cell plasma membrane with the virus outer envelope, the protein-based viral nucleocapsid (containing the viral DNA) is transported to the host cell nucleus, where components of the viral particle inhibit macromolecular synthesis by tire host cell. Herpes viral DNA and new viral nucleocapsid synthesis occurs within the host nucleus, with the acquisition of new viral envelopes via a budding process through the inner membrane of the host nucleus. The mature newly synthesized viral particles are subsequently... 

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