By Alexander Bernstein
Each year, nearly 200 million people come in contact with Malaria. The World Health Organization (WHO) establishes that as of June 2011, this disease is the fifth leading cause of death in the world among low-income countries, accounting for 5.2% of all deaths or nearly half of a million people each year. Such devastation is mostly concentrated in Sub-Saharan Africa as the Malaria Consortium organization relates that nearly 89% of the near 900 thousand million malaria-caused deaths occur in this region. Although less poignant than the toll on human life, the financial burden of this disease is also consequential. While an estimated 1.7 billion dollars are spent each year to combat malaria, this number only constitutes a third of the financial commitment that the 2009 WHO World Malaria Report suggests is required to effectively lower the disease’s exposure by 75% by the year 2015.
As with any ailment, it is important to understand how it functions. What causes malaria, and why is it so devastating? The answer can be found in an unlikely partnership between the female Anophelesmosquito and the Plasmodium parasite. After about a week incubation period in the mosquito, the parasite becomes readily transmitted to a human host. Once inside a new subject, the Plasmodium, the most dangerous variety of which is P. falciparum, resides and multiplies in the liver from anywhere between several weeks and several months. Then, the parasite invades the red blood cells and its presence becomes manifest. For the fortunate individuals with uncomplicated malaria, ailment is generally limited to fever, swelling, and typical flu-like symptoms. For the less fortunate, however, severe malaria takes hold, and fatal blood abnormalities and organ failures are not uncommon.
Although progress has been made dealing with this disease, most current treatments focus on the prevention of heme crystals through the introduction of competitive inhibitors. However, such treatments that attempt to assist the immune response are becoming less effective as the parasite continues to evolve slight differences. A new methodology is necessary. Luckily, researchers from Imperial College London and CNRS of France think they might have the answer. These scientists have determined what they define as the “Achilles Heel” of the parasite: its transcription process. Two separate transcription inhibiting molecules have been determined. Initial ex-vivo experiments have shown that the introduction of these molecules attacks the parasite during its longest life stage and is therefore incredibly effective at killing the Plasmodium. Primary Imperial College London Researcher Matthew Fuchter is extremely optimistic about future prospects as he explains that early results indicate the new treatment’s ability to “rapidly kill off all traces of the parasite, acting at least as fast as the best currently available antimalarial drug.” Importantly, these novice molecules also address the issue of resistant parasites, as they appear to effectively deal with even the most resilient and rapidly adapting Plasmodiumstrains. Fuchter and his colleagues from France have been extremely pleased with these results and maintain that a cure for Malaria will be found within the next decade.