Why mosquitoes don’t die of malaria

The risk of malaria looms over nearly half the world’s population and kills hundreds of thousands of people each year. But how do mosquitoes – which transmit the parasites that cause the disease – survive?

A team from the National Institute of Allergy and Infectious Diseases in the US has found how.

They uncovered a component of a mosquito’s immune system that allows the insect to withstand malaria-causing parasites.

Their work, published in Science Immunology, could lead to new ways of combating malaria transmission – and even help better understand chronic inflammatory diseases.

“The exciting thing about studies of this nature is that they start to delve into the complexity of the relationship between parasites and mosquitoes,” Cameron Webb, a clinical entomologist from the University of Sydney in Australia and who was not involved in the study, says.

“When we get into these really fine details, that’s when we start to identify weaknesses that can be exploited.”

Malaria is caused by single-celled Plasmodium parasites. When a person is bitten by an infected mosquito, the microbe makes its way through the host’s bloodstream to the liver where it replicates, returns to the blood and infects red blood cells.

But mosquitoes don’t have red blood cells – their blood is a somewhat colourless fluid containing the blood cell equivalent called haemocytes – so the parasites instead escape to the mosquito’s saliva from the gut.

In an interview with the American Association for the Advancement of Science, study co-author Carolina Barillas-Mury says she and her colleagues knew from indirect evidence that haemocytes were somehow involved in the battle against the parasites.

But details were few and far between.

So she and her team took Anopheles gambiae, a sub-group of mosquitoes responsible for most malaria cases in Africa, and, using a fluorescent dye, tracked their behaviour in the presence of Plasmodium.

They saw the haemocytes shed specks of plasma membrane known as microvesicles. This activated a cascade of proteins which targeted and destroyed the infection-causing microbes.

So how does this information help us?

First of all, the researchers noticed that the haemocytes behaved similarly to the vertebrate immune system when under threat. For instance, they triggered inflammation, just like our cells do.

And when the process is chronically activated in humans, it can lead to inflammatory diseases such as atherosclerosis and rheumatoid arthritis.

Barillas-Mury says these findings will help better understand how chronic inflammatory diseases occur, perhaps leading to new prevention therapies that target the source of the problem.

Secondly, by learning what keeps the mosquitoes blind to a parasite invasion, the researchers can develop what’s known as a “transmission blocking vaccine”. 

Barillas-Mury says malaria parasites harbour a gene that renders them invisible to mosquitoes.

“Parasites are masters of decoy. We can take advantage of a system already in place – the mosquito has all the tools to kill the parasite, but the parasite is blocking the mosquito.”

Genetic modification can make the parasite visible to the mosquitoes’ immune system, allowing them to kill the parasites once infected instead of spreading it to humans.

Webb says malaria is primarily tackled by eradicating malaria-carrying mosquitoes, but this could have consequences on the wider food web.

Genetically modifying mosquitoes, though, might work on a larger scale.

“You can avoid that debate if you don’t actually eradicate the mosquito, but change them to a point where they’re no longer transmitting those parasites,” Webb says.

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