Viagra May Prove a Valuable Weapon Against Malaria



By Pablo Correa Torres
The male impotence drug Viagra could also prevent malaria transmission, an in-vitro study demonstrates.
The drug stiffens red blood cells infected with malaria. This should cause them to be removed from the blood by the spleen as part of its role in destroying old red blood cells and preventing them from being taken up by mosquitoes when they bite.

 While this would not treat malaria in those already infected, it could reduce the disease's spread, say the authors of a paper published last month in PLOS Pathogens.
Gordon Langsley, a researcher at the Cochin Institute in France and member of the team that undertook the study, tells SciDev.Net that the work demonstrates how drugs like Viagra could be novel ways to block malaria transmission.

The scientists used Viagra to target the first part of the life cycle of the malaria parasite Plasmodium, which takes place in humans. If an infected person is bitten by a mosquito, the parasite incubates inside the mosquito and is passed on to people it bites.

But when exposed to Viagra, the infected cells became rigid, meaning they would be unable to pass through the spleen's blood filter and so would be removed from the bloodstream, the researchers say, potentially preventing the infection's spread.

According to the World Health Organization, there were around 198 million cases of malaria in 2013, when about 584,000 people died from the infection. Common methods to control the spread of the disease include using mosquito nets, insecticide and reducing breeding grounds of mosquitos near humans. But there are no widely available drugs to prevent transmissions once the infection is in a human host.
However, there also remains the issue of addressing the symptoms of malaria, says Socrates Herrera-Valencia, director of Caucaseco Scientific Research Center in Colombia. "This discovery opens a path to cut infection among humans, but not to treat the symptoms of an infected patient," he says.
Other scientists say the study may one day help to contain malaria, but many hurdles remain before any resulting drug could be prescribed.

"It is not a weakness of the study, but we must call attention to the fact that it is a work in vitro, in the laboratory," says Diego Golombek, a biologist at the National University of Quilmes in Argentina. "We don't know if the mechanism can be maintained in an in vivo model."


References
Ghania Ramdani and others cAMP-signalling regulates gametocyte-infected erythrocyte deformability required for malaria parasite transmission (PLOS Pathogens, 7 May 2015)


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