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Two groups of Howard Hughes Medical Institute (HHMI) scientists working independently have identified a critical enzyme that allows the malaria-causing parasite, Plasmodium falciparum, to take over and thrive in human red blood cells.
The enzyme plasmepsin V (PMV) is a gatekeeper inside the malaria parasite that allows the parasite to export its own proteins into a human red blood cell. Once PMV opens the gate into the red blood cell, the parasite moves hundreds of the proteins into cell, which remodels it and, eventually, annihilates it. The new observations demonstrate that PMV is critical to survival of the malaria parasite and suggest that drugs targeting PMV may be able to kill the parasite before it develops inside red blood cells. This research was published by HHMI international research scholar Alan Cowman and HHMI investigator Daniel Goldberg in two articles in the February 4, 2010, issue of Nature.
Malaria affects between 350-500 million people worldwide each year and kills between 1 to 3 million of them, according to the Centers for Disease Control and Prevention. Malaria parasites go through a series of steps on their way to causing disease in humans. When a malaria-carrying mosquito bites a human host, the malaria parasite enters the bloodstream, multiplies in the liver cells, and is then released back into the bloodstream, where it infects and destroys red blood cells. Parasites invade red blood cells in an attempt to evade the immune system and to remodel them for their own use.
Former studies could demonstrate that platelets can kill parasites in the Petri dish and in mice.
In fact, previous studies suggested that platelets might make the disease worse
by causing cerebral malaria, a potentially lethal complication.
But Foote’s research presents a different picture- -showing that platelets actively fight malaria infection.
Platelets are well known for their role in blood clotting and blood vessel repair.
Previous studies have shown that platelets are
active in the
body’s innate immune systemwhich responds rapidly to invading pathogens.
Innate immunity is complemented by the adaptive immune system, which kicks in later and has the amazing ability to recall the specific molecular features of any pathogen it has encountered in the past.
The innate immune response is particularly important in fighting malaria, which causes symptoms once the parasite has invaded the victim’s red blood cells.
There are several types of malaria –
each caused by a different type of parasite--
so infection with one type does not train the adaptive immune system how to fight against another form of malaria.
“From a biological perspective,
I think this finding is likely to be very important in understanding the host’s response to infection by malarial parasites,” Foote said.
“We think that platelets are one of the major factors that prevent people from dying early on in a malarial infection.”
When Foote and his colleagues began their experiments,
platelets were not their interest.
He and postdoctoral fellow Brendan McMorran
were examining whether genetic mutations make malaria-resistant mice susceptible to the disease.
During those studies, they discovered that platelet-deficient mice were much more likely to die of malaria than mice with normal platelets.
They used a specific type of mouse that was missing the Mpl gene.
As a consequence of that mutation, the mouse produced just one-tenth the normal amount of platelets.
When these platelet-deficient mice were infected
with Plasmodium chabaudi,
a rodent version of the malaria parasite, half of the females and
all of the males died of malaria.
Only five percent of females and 20 % of males with normal platelet counts died.
“The entire project stemmed from that original observation,” Foote said.
That accidental finding led Foote and his colleagues to ask whether platelets had a direct role in malarial infection.
To ensure that their original observation was not due to other genetic changes caused by knocking out
the Mpl gene, the researchers eliminated platelets by giving the mice aspirin, which inactivates platelets.
They found that the aspirin-treated mice were also much more likely to die of malaria.
Although there is more work to do, the researchers believe that the aspirin is preventing some sort of anti-malarial effect produced by the platelets.
Using the mouse models, the researchers couldn’t directly see how the platelets interacted with the parasites.
So they conducted similar experiments in a Petri dish in which they added human platelets to red blood cells infected with Plasmodium falciparum,
the most deadly human malaria parasite.
Those studies showed that the platelets were indeed killing the parasites.
And when aspirin was added, the platelets no longer held back the parasites.
“Out of this entire work,
the most practical outcome is
that one should seriously re-investigate
whether aspirin is really a good antipyretic
[fever-reducing] drug to use in the context
of a malarial infection,” Foote said.
Foote cautions that the current experiments were done
in mice, but he said they may have some relevance for understanding how humans respond to malaria infection.
For example, low platelet counts are often seen in
malaria patients in the early stages of infection.
We believe that’s because platelets bind
to infected red blood cells and are taken out
of circulation because of that,” Foote said.
“What we think is happening during those first few days of malarial infection is that platelets are actually a buffer against rapid growth of malarial parasites.
We definitely see this in mouse experiments.
Foote says this means platelets are part of the innate response to malarial infection.
But how platelets are actually able to kill the parasites is still unclear
and will be the subject of future research.
“There will still be quite a lot to do in the field to show that this would really have some effect in humans in the real world,” he acknowledged.
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