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Dissecting the molecular interaction between hepatocytes and Plasmodium liver parasites
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Malaria is one of the world´s leading causes of death, responsible for
over 700,000 deaths per year, the majority of which are African children under
5 years of age. Malaria disease is caused by the transmission of an
Apicomplexa parasite, Plasmodium, through the bit of a female Anopheles
mosquito, and transmitted parasites quickly reach the mammalian host liver,
where the first round of replication begins.
Plasmodium sporozoites, once inside the liver, must invade and survive
within hepatocytes until the first replicative stage within the mammalian host is
accomplished. Upon migration through various cells, sporozoites are able to
actively enter hepatocytes, forming a Parasitophorous Vacuole Membrane
(PVM) around itself. Once this intracellular niche is established, parasite
replication and growth is initiated. Dramatic morphological as well as gene
expression modifications occur at this stage, and the parasite achieves one of
the highest replication rates known within eukaryotic species (Sinnis and Sim,
1997).
Although the Plasmodium life-cycle has been extensively
characterized, relatively little is known about sporozoite interaction with host
organelles, vesicles and proteins. To address this issue, Plasmodium
interactions with the host cell endomembranes was analyzed at various stages
of liver infection using indirect immunofluorescence. Plasmodium parasites
were seen closely associated with host endoplasmic reticulum (ER) and the
Golgi apparatus. Surprisingly, late endosomes/lysosomes, observed with the
membrane markers Rab7a, CD63 and LAMP1, aggregated around the parasite.
No interaction with host peroxisomes, early and recycling endosomes was
observed.(...)
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Dissertation presented to obtain the Ph.D degree in Biology
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Universidade Nova de Lisboa. Instituto de Tecnologia Química e Biológica