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Our laboratory has defined an evolutionarily conserved role for autophagy genes in innate immunity against viruses and bacterial infections. Present studies are aimed at understanding: (1) how intracellular pathogens are recognized by the autophagic machinery; (2) how autophagy limits viral replication and intracellular bacterial multiplication; (3) how autophagy regulates cell death and cell survival in infected cells and tissues; (4) whether declines in autophagy function with aging contribute to age-related increases in susceptibility to infectious diseases; (5) which strategies intracellular pathogens use to evade host autophagy; and (5) the role of viral evasion of autophagy in viral pathogenesis, including acute infection and chronic medical diseases (e.g. cancer and neurodegenerative diseases). To accomplish these goals, we are currently studying two viruses that infect the central nervous system and cause lethal encephalitis, Sindbis virus, and herpes simplex virus; a murine gammaherpesvirus that provides a model for human oncogenic gammaherpesviruses; and the intracellular bacteria, Salmonella typhimurium, an important cause of enteric infection. We are employing a variety of cell biology, biochemistry, and genetic approaches in tissue culture and animal model systems to understand the role of autophagy in combating these pathogens, and the role of autophagy evasion in microbial pathogenesis. The principles that we uncover in our studies of these organisms are likely to have broad relevance to a variety of different intracellular pathogens and result in new ways of thinking about host-pathogen interactions and the pathogenesis of infectious diseases. (View image) |
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