Researchers have discovered it is possible to slow the development of the malaria
parasite inside blood cells by altering its gene expression. They suggest that even drug-resistant
strains, which are on the increase worldwide, may succumb to this technique.
The technique even slowed parasite development in strains that have
developed resistance to common anti-malaria drugs.
The team, from Yale University in New Haven, CT, reports its findings in the
Proceedings of the National Academy of Sciences.
While huge gains have been made in the global fight to eradicate malaria, the disease
still devastates lives and livelihoods, particularly in Africa, where nearly half a million
children under the age of 5 die of the parasitic disease every year.
Effective tools to prevent and treat malaria do exist, but the emergence of parasite
strains that are resistant to drugs and insecticides threatens to undermine hard-won
“Drug resistant strains are becoming a very serious problem in places like
Southeast Asia,” notes senior author and Nobel laureate Sidney Altman, a molecular biologist and professor at
People become infected with malaria through bites from female mosquitoes carrying a
parasite called Plasmodium. Once inside the human body, the parasite multiplies in
the liver then infects red blood cells.
If not treated quickly, malaria can become life-threatening by disrupting blood supply to
vital organs. Every year, nearly 2 million people are sickened by malaria, and 600,000 die from the disease.
In their study paper, Prof. Altman and colleagues highlight the importance of
understanding the biology of the malaria parasite, particularly its genes, as this could be
a fruitful avenue for finding new drug targets.
New technique targets RNA to alter gene expression
Their work relates to the role of RNA (ribonucleic acid), which carries instructions from DNA for directing the synthesis of proteins that are crucial to the
organism’s growth and development.
In the study, the researchers found a way of easily altering the gene expression of
Plasmodium falciparum – the most deadly of the malaria parasite strains known to infect humans – by
The tool that they used to alter the expression of P. falciparum by RNA is called
a morpholino oligomer (MO). Researchers use MOs to block the access of other molecules to
specific sequences in RNA.
Prof. Altman and colleagues showed it is possible to use MOs to interfere with gene
expression in P. falciparum in such a way that they disrupt the organism’s
development inside blood cells.
The team demonstrated that the technique slowed parasite development even in strains that have
developed resistance to two common anti-malaria drugs. In their paper, they conclude:
“The ease in design of the MO molecules presents a possibility for their use
in large-scale genome functional analyses and possibly in malaria therapy.”
In 1989, Prof. Altman was awarded the Nobel prize for discovering that RNA is also
involved in helping chemical reactions in cells in a similar way to an enzyme. Before then, it was thought
that only proteins could behave like enzymes and that RNA’s role was limited to carrying
genetic codes between parts of the cell.
Meanwhile, Medical News Today reports how the crime scene compound luminol could help fight malaria. A team from Washington
University in St. Louis found that the chemical – which crime scene detectives use to
illuminate tiny blood particles – triggers an amino acid in hemoglobin that can kill P.
falciparum in red blood cells.
Written by Catharine Paddock PhD
Copyright: Medical News Today
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