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The endosymbiont  Wolbachia w AlbB induces refractoriness to  Plasmodium falciparum  in  Anopheles stephensi , the primary mosquito vector of human malaria in the Middle East and South Asia. However, it remains unknown whether such refractoriness can be extended to other malaria species. In particular, it was reported that under very specific conditions,  w AlbB can enhance  Plasmodium  infection in some hosts. Here, we measured the impact of  w AlbB on the rodent malaria parasite  Plasmodium berghei  in  A. stephensi  by comparing the load of oocysts and sporozoites in midguts and salivary glands, respectively, between  w AlbB-infected and -uninfected mosquitoes. To investigate whether  w AlbB modulated mosquito immune defense against parasites, we compared the expression of the immune genes, which were previously reported to involve in antimalarial response, in both midguts and the remaining carcass tissues of mosquitoes. The stable association of  w AlbB with  A. stephensi  resulted in reduction of parasites by more than half at the oocyst stage, and up to 91.8% at the sporzoite stage. The anti- plasmodium  immune genes, including  TEP1 ,  LRIM1 , Toll pathway gene  Rel1  and the effector  Defensin 1 , were induced by  w AlbB in different mosquito body tissues. These findings suggest that immune priming is a potential cause of  w AlbB-mediated antimalarial response in  A. stephensi . More importantly, no evidence was found for any enhancement of  Plasmodium  infection in  A. stephensi  stably infected with  w AlbB. We discuss these findings with possible implementations of  Wolbachia  for malaria control in disease endemic areas.

The Maternally Inheritable Wolbachia wAlbB Induces Refractoriness to Plasmodium berghei in Anopheles stephensi