Could Viagra help stop the spread of malaria? A new study by a team of European scientists makes it look like a possibility worthy of further consideration.
According to the World Health Organization, malaria killed an estimated half a million people in 2013. One obstacle in slowing the spread of the disease is the fact that even patients whose symptoms have resolved may still be contagious for days to weeks. Viagra won’t cure the disease, but it might be able to stop the spread of malaria from patients to mosquitos and, from there, to other people.
In humans, Viagra blocks the cell’s ability to break down a molecule called cyclic GMP, or cGMP. When cGMP builds up in the muscle cells that line blood vessels, those blood vessels relax and blood flow increases. In fact, Viagra was originally developed as a blood pressure medication. Researchers stumbled upon what we now consider its primary use when patients in a clinical trial started reporting erections as a side effect.
Single-celled malaria parasites don’t have blood vessels, and they don’t get erections. But they do have some of the same cellular machinery, and they can get stiff. What this new study shows is that Viagra causes the build-up of a similar molecule – cyclic AMP, or cAMP - in the sexual, or reproductive, stage of malaria parasites. That excess cAMP changes the outer membrane of both the malarial cells and the human red blood cells they infect, causing them to become more rigid.
That’s serendipitous, because it may enable the spleen to capture and destroy malaria-infected cells the same way it usually does old or damaged red blood cells. The spleen is like a mesh whose main job is to filter the blood. Healthy red blood cells are soft and squishy enough to squeeze through. Old or damaged red blood cells are stiffer, and get caught. In this new study, mesh filters did the same to malaria-infected red blood cells that had been treated with Viagra.
Of course, it’s a long way from mesh filters to human patients. The next step is to test Viagra’s effectiveness against malaria in mice and then humans, which senior author Catherine Lavazec says they’re hoping to do next year. They’re also hoping to find a way to modify the active ingredient in Viagra, so that it still makes the infected red blood cells stiffen up, but doesn’t do the same to other parts of the human body.
If it all works out, this could be an important development in efforts to eradicate malaria. If the spleen can remove sexual-stage malaria from the blood, then the next mosquito who comes along can’t pick up the parasite and pass it to someone else. That breaks the chain of transmission.
Matt Marti, a malaria researcher at Harvard’s School of Public Health, says it’s only been in the past decade or so that researchers have realized how critical that is to eliminating the disease. The anti-malarial drug primaquine can block transmission, but it can cause severe and potentially fatal anemia in patients with a genetic disorder, called G6PD deficiency, which primarily occurrs in areas where malaria is found. Beyond that, Marti says most efforts to target the transmission process have focused on clearing malaria out of mosquitos – a difficult and inefficient approach. In contrast, Marti says stopping the cycle in humans – the way Viagra might – is timely and a “perfect target.”
