| Summary: | Includes bibliographical references === [No subject] Malaria infection caused by the apicomplexa pathogen Plasmodium falciparum has a high rate of resistance to existing anti-malarial drugs. The World Health Organisation recommended interventions are unlikely to eliminate the growth of resistance and it would therefore be prudent to continue the search for new drug targets for the continued combatting of malaria. Plasmodium falciparum is parasitic on the host for its metabolites and therefore inhibiting the transportation of glutamine from the host, has long been considered a potential strategy for combating the spread of infection. The recently sequenced Plasmodium falciparum genome has however shown that pathways for independent survival are also conserved. Therefore, combating the spread of Plasmodium falciparum in the human host, in addition to inhibiting the transportation of glutamine, will also require the inhibition of the de novo expression of essential amino acids within the Plasmodium falciparum cell. This could be achieved by inhibiting the glutamine synthetase gene, which is an essential step in the tri-carboxylic acid cycle.
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