Interaction between host cell mitochondria and Coxiella burnetii.

In order to successfully establish a replicative niche, intracellular bacterial pathogens must influence eukaryotic cell biology. Vesicle and protein traffic, transcription and translation, metabolism and innate immune signaling are all important elements of the host-pathogen interaction that can be manipulated by intracellular bacterial pathogens. The causative agent of Q fever, Coxiella burnetii, is a mammalian adapted pathogen that replicates in a lysosome-derived pathogen-modified vacuole. C. burnetii establishes this replicative niche by using a cohort of novel proteins, termed effectors, to hijack the mammalian host cell. The functional and biochemical roles of a small number of effectors have been discovered and recent studies have demonstrated that mitochondria are a bona fide target for a subset of these effectors. Various approaches have begun to unravel the role these proteins play at mitochondria during infection, with key mitochondrial functions, including apoptosis and mitochondrial proteostasis, likely influenced by mitochondrially localized effectors. Additionally, mitochondrial proteins likely contribute to the host response to infection. Thus, investigating the interplay between host and pathogen elements at this central organelle will uncover important new understanding of the C. burnetii infection process. With the advent of new technologies and sophisticated omics approaches, we are poised to explore the interaction between host cell mitochondria and C. burnetii with unprecedented spatial and temporal resolution.