Computational Biology and Chemistry
The Lucy Family Institute uses computational biology and chemistry to help identify:
- novel protein functions
- disease and pathogen-interacting genes
- drug targets
- evolutionary conserved interactions and protein complexes
- missing and wrongly reported interactions
- reconstruction of species phylogeny
- understanding mechanisms of pathogenicity
- drug resistance
- phenotypic variation
Lucy Family Institute researchers apply computational methods to other research domains as well. In computational chemistry and synthetic biology, the proposed methods can analyze network representations of proteins structures and drug compounds, hence deepening our understanding of protein stability and folding and leading to more efficient drug design. In the context of ecological systems and climate change, the methods can study population dynamics, interactions between species, and ecological processes responsible for species' environmental adaptation to global climate change.
Understanding the Role of Transmission Heterogeneity in Parasitic Worm Diseases
Researchers study Onchocerciasis (river-blindness) and lymphatic filariasis. These diseases are black-fly and mosquito-borne neglected tropical diseases that cause blindness and elephantiasis in humans. Onchocerciasis affects approximately 37 million people in Latin America, Africa, and the Arabian peninsula. Lymphatic filariasis affects approximately 120 million people worldwide and is endemic in 72 countries. The primary control strategy for these diseases consists of mass drug administration and vector control. Mass drug administration programs provide people in infected areas with chemotherapeutic drugs which kill the parasitic worms in patients, while vector control attempts to prevent black-flies and mosquitoes from biting humans through insecticides and bed nets. With this research, researchers are determining which combinations and what durations of these intervention techniques are most effective at eradicating the disease.
Genetics and Genomics of Drug Resistance
Drug resistance is best understood not as a simple single gene mechanism, because even major drug resistance genes function in the context of other genes, making genetic backgrounds important. Researchers are evaluating the extensive relationships that exist among malaria parasite drug susceptibilities and growth rates that reflect genome-wide co-adaptive processes and overlapping genetic mechanisms. Natural genetic variability, as displayed by genetic crosses and outbred populations, provides valuable views of these co-adapted systems.