Malaria vaccine passes early human trial

A malaria vaccine that used a genetically weakened form of the parasite, with reduced virulence, has passed clinical trial with human volunteers, researchers say.

The findings, published in the journal Science Translational Medicine, showed that the vaccine is well tolerated and stimulates an appropriate immune response as well as provides a path forward for highly protective malaria vaccine.

"The clinical study now shows that the vaccine is completely attenuated in humans and also shows that even after only a single administration, it elicits a robust immune response against the malaria parasite. These findings are critical milestones for malaria vaccine development," said Sebastian Mikolajczak, principal scientist at Center for Infectious Disease Research (CIDR) -- a non-profit research organisation in the US.

Malaria is caused by Plasmodium parasites that are transmitted to humans by a mosquito bite and first infects the liver and then the blood, leading to over 200 million infections and nearly a half-million deaths worldwide in 2015.

In the trial, conducted in 10 healthy volunteers, the researchers used a genetically engineered malaria parasite that is weakened by removal of three specific genes that are required for the parasite to successfully infect and cause disease in humans.

These genetically attenuated parasites, or "GAPs", arrested the development of the parasite within the liver, thereby preventing its advance to blood infection, the stage of malaria that triggers disease symptoms.

The GAP3KO vaccine was administered through infected mosquito bites in a controlled setting.

The participants, none of whom developed malaria symptoms or signs of infection in the blood, showed strong protective antibody responses. When transferred into humanised mice, these antibodies blocked malaria infection in the liver.

These promising results pave the way to a phase 1b trial of the GAP3KO vaccine candidate using controlled human malaria infection, the researchers noted.

--IANS

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