Lymphatic filariasis is a neglected tropical disease caused by three different species of parasitic worm, which are spread between human hosts by mosquitos. The molecular interactions between the worm, mosquito, and human are dynamic and delicately balanced, suggesting that disrupting these interactions might be an avenue for the development new therapeutic treatments. The worm Brugia malayi (image), one of the parasites that causes elephantiasis, develops as larvae inside the mosquito vector until it reaches the infective L3 stage at which point it is transmitted back into a human host when the mosquito takes a blood meal. The adult worms live and mate within the human lymphatic system while offspring are shed into the bloodstream to be picked up again by mosquitoes. While the life-cycle is well documented it has been difficult to define the exact molecules that the parasite uses to control its hosts. Research has traditionally searched for secreted proteins and, while there are several candidates, along with proteins expressed on the surface of the parasite that may play a part, recent research, carried out by scientists at Iowa State University, together with collaborators at Northewestern University, the University of Georgia, and the University of Wisconsin-Madison, has revealed that small non-coding RNAs carried in exosome-like vesicles (ELVs) may also be involved in controlling the host’s response to the parasite. This new research was published online on September 24, 2015 in the open-access journal PLOS Neglected Tropical Diseases.
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