RIBONUCLEOTIDE REDUCTASE. My long-term objective is to understand human disease transmission by blood-feeding insect vectors. I am specifically interested in the role that iron plays during pathogenic invasion. Data in vertebrates suggest that pathogenic infectivity may be linked to the availability of iron in the host. In vertebrates, some iron-binding proteins are upregulated under pathological conditions. This upregulation is hypothesized to cause chelation of iron and thus reduce iron availability to the pathogen. The actual machinery that activates this response remains unknown. My aim is to elucidate the mechanisms by which pathogenic infectivity is affected by the host iron metabolism. The host organism for my research is the hematophagous (blood feeding) mosquito, a vector of numerous diseases. Worldwide, millions of people die yearly from diseases transmitted by hematophagous insects. In the U.S., for the past few years, the West Nile virus carried by the mosquito Culex pipiens has caused epidemic outbreaks nationwide and cost the U. S. hundreds of thousands of dollars; West Nile virus is moving westward and southward. With all the public health concerns, not much is known about the basic biology of hematophagous insects. My work has a foundation for understanding how these disease vectors regulate their iron metabolism.
