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This review aims to discuss the computational approaches used till date to construct a malaria protein interaction network and to catalog the functional predictions and biological inferences made from analysis of the PPI network.
Here, we combined immunofluorescent microscopy, biochemical assays, in silico prediction, and mass spectrometry analysis using the multidimensional protein identification technology, or MudPIT, to describe the P. falciparum ubiquitome.
Comparing the modeling results with a comprehensive list of known drug targets for P. falciparum, showed that we had the best discovery success with a network model consisting only of enzymes from the parasite alone which coding genes were known.
Recent studies using molecular approaches demonstrated that wild and captive gorillas and captive bonobos and chimpanzees are infected with P. falciparum and that these apes harbor parasites broadly related to P. falciparum.
Here, we used single genome amplification (SGA) strategies to show that wild-living African apes are naturally infected with at least nine Plasmodium species, including one that is the direct precursor of P.falciparum.
Despite prolonged and intense effort to understand and control the health impact of malaria morbidity and mortality, malaria remains third in the global ranking for severe and fatal infections.
The available data are thus most consistent with the hypothesis that P. reichenowi (in the strict sense) and P. falciparum co-speciated with their hosts about 5–7 million years ago.
No abstract available.
Plasmodium knowlesi is now established as the fifth Plasmodium species to cause malaria in humans.
We investigated here the hypothesis that the delayed acquisition of immunity to malaria could be related to a worm-induced Th2 drive on antimalarial immune responses.