Fatty molecules in blood controls malaria parasites

Depletion of a fatty molecule in human blood propels malaria parasites to stop replicating and causing illness in people Plasmodium falciparum is the parasite responsible for malaria. The key molecule the researchers identified has the catchy name of lysophosphatidylcholine LPC. It appears to be a building block the parasites use to construct new cell membranes when they divide. When LPC drops, the parasites can't multiply anymore and commit to a different pathway, but multiply when LPC increases.

Treating patients with antimalarial drugs usually kills the replicating parasites, but if you don't also block transmission, the disease will never disappear from the population, they pass into humans through the bite of an infected Anopheles mosquito, congregating first in the liver and later in red blood cells, where they multiply and burst forth in cycles that cause waves of illness.

If the host survive, some of the parasites stop multiplying and follow a different path known as sexual commitment or differentiation. If mosquitoes bite an infected person during this phase, the parasites-now male and female-travel back into the insects and breed. The transmission cycle begins afresh.

When the researchers cultured Plasmodium cells in flasks without their usual bath of human blood serum, the parasites skipped replication and went straight for sexual commitment-hinting that a control switch lurked in the missing blood. The researchers grew Plasmodium with serum. As expected, after a while the parasites lost their zest for replicating and began to undergo sexual commitment. But when the team added fresh serum, the parasites went on replicating. They were indeed grabbing something from the serum.

The researchers decided to separate and study all the serum components to see if they could identify the molecule or molecules at play. We found a single factor that's necessary and sufficient for regulating sexual commitment with each round of parasite replication, the researchers observed that LPC levels dropped. When LPC fell low enough, the parasites switched to sexual commitment.

Plasmodium cells were absorbing LPC from the bloodstream as they prepared to divide. The scientists believe that when the parasites sense that their raw materials are running low, they change strategies. The researchers found similar patterns of LPC depletion in a mouse model of malaria.
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Human red blood cell receptor prevents malaria

Researchers have discovered that protection from the most severe form of malaria is linked with natural variation in human red blood cell genes.

A study from the Wellcome Trust Sanger Institute, the Wellcome Trust Centre for Human Genetics and their collaborators has identified a genetic rearrangement of red blood cell glycophorin receptors that confers a 40 percent reduced risk from malaria.

The most widespread malarial parasite in Africa is Plasmodium falciparum.
Plasmodium parasites infect human red blood cells and gain entry through receptors on the cell surface.

Researchers investigated the glycophorin area of the genome in more detail than before using new whole-genome sequence data from 765 volunteers in the Gambia, Burkina Faso, Cameroon, and Tanzania.

Using this new information they then undertook a study across the Gambia, Kenya, and Malawi that included 5310 individuals from the normal population and 4579 people who were hospitalised from severe malaria.

They discovered that people who have a particular rearrangement of the glycophorin genes had a 40 percent reduced risk of severe malaria. This  shows that that people with complex rearrangement of GYPA and GYPB genes, forming a hybrid glycophori may not develop severe complications malaria.

The hybrid GYPB-A gene is found in a particular rare blood group - part of the MNS blood group system - where it is known as Dantu. The study found that the GYPB-A Dantu hybrid was present in some people from East Africa, in Kenya, Tanzania, and Malawi, but that it was not present in volunteers from West African populations.

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