Scientists announce malaria breakthrough
Malaria kills about 800,000 people a year, most of them children in sub-Saharan Africa. And, while researchers haven’t found a cure, they’ve made a huge leap in our understanding of how the disease works - one that could finally lead to an effective vaccine. By SIMON ALLISON.
Before you can cure a disease, you must understand how it works. Much of the multibillion-dollar industry of vaccine development is not focussed on dreaming up a vaccine, but on discovering how a disease enters and then functions in the human body. Once that’s understood, a cure can be contemplated.
That’s why the breakthrough announced by scientists from the Sanger Institute is so important. They’ve been able, for the first time, to pinpoint exactly how malaria enters the bloodstream. Once you’re bitten by the carrier mosquito, the researchers discovered that the malaria parasite relies on a single protein receptor to gain entry to the red blood cells where it multiplies. Once it’s in the blood, it becomes dangerous to humans. Knowing how this process works might mean drugs can be developed to target the particular protein receptor, which researchers describe as the “lock” into which the malaria parasite inserts its “key” to enter. All they need do now is change the lock.
“Our research seems to have revealed an Achilles heel in the way the parasite invades our red blood cells,” said Gavin Wright, co-leader of the study. “Our findings were unexpected and completely changed the way in which we view the invasion process. The great hope is that this breakthrough will facilitate the path towards a more effective vaccine.” This could still take a long time – up to a decade – but it’s an important new direction for researchers.
This is the second major development around malaria this year. Last month pharmaceutical company GlaxoSmithKline released the test results of its experimental RTS,S vaccine, which appeared to halve the risk of malaria in children. DM
- Malaria: beginning of the end? in the Independent.