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Scientists Pinpoint Treatment Soft-spot For Severe Malaria 

By Divine Ntaryike Jr — Researchers at the University of Edinburgh in the UK are jubilating.  They have pinpointed a connection between different species of malaria parasites that cause life-threatening forms of the disease.

Malaria is transmitted by the bite of bloodsucking mosquitoes.  When they bite, they secrete parasites called protozoans which initially travel to the liver where they multiply and are eventually discharged into the bloodstream to launch assaults on red blood cells.

The parasites rely on precise receptors on the surface of the red blood cells to invade.  They attach a protein – essential constituents of living cells – to the receptor to unbolt the doorway and penetrate the red blood cell.  Once inside, they mature and reproduce, causing possibly deadly disease.

There are four main strains of malaria of the Plasmodium genus which infect humans – P. falciparum, P. vivax, P. ovale and P. malariae. The most serious of these is the falciparum which can be very fatal. 

The scientists at the University of Edinburgh’s School of Biological Sciences have identified a key protein they say is common to the fatal strains of malaria.  According to a report of the findings published April 21 in PLoS Pathogens, they have also found that antibodies or proteins normally present in the body or produced to provide immune responses to attacks by targeting the malaria parasites’ protein are effective against the severe malaria strains. 

They say once in the bloodstream, the parasites “are able to alter the protein molecules on their surfaces to evade attack by the immune system. These surface proteins are usually poor targets for treatments or vaccines because they are highly variable between different malaria parasite strains.”

After binding to the red blood cells, the parasites form perilous clumps, otherwise called rosettes, which can block blood vessels leading to severe conditions like coma and brain damage. The researchers found that the surface proteins of the clump-forming parasites share similarities that may allow them to act as a target for treatments to block progress of malaria.

“We knew that clusters, or rosettes, of blood cells were found in many cases of severe or life-threatening malaria, so we looked at rosette-forming parasites and found a common factor that we could target with antibodies,” Professor Alexandra Rowe of the University of Edinburgh“s School of Biological Sciences, who led the study said.

The UK scientists collaborated with researchers in Cameroon, Mali, Kenya and Gambia to try their antibodies against parasites collected from patients in these countries.

It is hoped the finding will stimulate the development of vaccines or drugs against life-threatening cases of malaria.  “We hope this discovery will inform new treatments or vaccines to block the formation of rosettes and so prevent many life-threatening cases of malaria,” Prof Rowe concluded.

Severe malaria currently kills between 10 and 20 percent of victims.  In general terms, malaria kills some one million people worldwide yearly. 

Prof Rowe’s findings follow announcements late last year of a possible breakthrough in the search for malaria vaccines.  In December 2011, scientists at Oxford University announced they had developed a new vaccine which neutralizes all strains of the most deadly species of malaria parasite.

Dr Simon Draper of the Jenner Institute at the University of Oxford demonstrated that the developed vaccine induces an antibody response in animal models capable of counteracting all the tested strains of the P. falciparum parasite.

"Our initial finding was unexpected and completely changed the way in which we view how the malaria parasite invades red blood cells," said Gavin Wright, of the Wellcome Trust Sanger Institute, who co-authored the study that was published in the journal Nature Communications. "It revealed what we think is the parasite’s Achilles’ heel in the way it invades our cells and provided a target for potential new vaccines," he added.

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