Ana Beatriz Barletta Ferreira

I have a broad background in vector-borne diseases, focusing on the interaction of the mosquito immune system and several different pathogens to understand how it affects the outcome of transmission. Throughout my projects, I have worked with several different infection models, like Aedes aegypti and dengue virus, bacteria and fungi, and Anopheles gambiae and Plasmodium. During my master?s, I characterized the modulation of Aedes aegypti immune pathways in response to viral, bacterial, and fungal infections. I also established a collaboration with Dr. George Dimopoulos Lab to perform microarray analysis to understand how mosquito lipid metabolism contributes to fighting dengue infections. My Ph.D. project focused on the role of lipophilic organelles, known as lipid bodies, as part of the defense mechanism against the dengue virus in the mosquito Aedes aegypti. These organelles were well known in mammals, but our data was the first contribution that associates lipid bodies and immune responses in insects. My Ph.D. gave me a strong background in cellular and molecular biology and allowed me to work with different laboratory models of infection. I was awarded a competitive Brazilian fellowship that supported an internship of 2 years at the National Institutes of Health during my Ph.D. Under the supervision of Dr. Carolina Barillas Mury, I described prostaglandins (bioactive lipid) as a chemotactic signal that primes the mosquito immune system and turns Anopheles gambiae resistant to Plasmodium infection in a second encounter with the parasite. For my post-doctoral training, I return to Dr. Barillas-Mury lab at NIH, and my multidisciplinary expertise allowed me to establish internal collaborations at NIH and other institutes as USDA, UFRJ (Brazil), Fiocruz-MG and the Sanger Institute. Currently, my main project addresses how Anopheles mosquitoes perceive and respond to the oocyst presence in the midgut, and limit Plasmodium survival through a response that targets late stages of parasite development. Anopheles immune responses in early stages of Plasmodium infection, culminate with the activation of the complement system, resulting in massive parasite killing. Parasites that survive initial reactions differentiate into oocysts and grow continuously under the midgut basal lamina for up to twelve days, quiet and unnoticed, until rupture and release of sporozoites that invade the salivary gland completing the transmission cycle. Plasmodium oocysts are thought to be a ?quiet? stage that develops unnoticed by the mosquito for several days. Using a transgenic Anopheles stephensi mosquito strain, my project investigates the role of midgut remodeling and renewal in response to the oocyst presence, and this impacts parasite survival and malaria transmission.