Abstract
Coxiella burnetii, the causative agent of human Q fever, is an obligate intracellular bacterial pathogen that replicates in a large, membrane-bound vacuole known as the Coxiella Containing Vacuole (CCV). The CCV is a unique, phagolysosome-derived vacuole with a sterol-rich membrane containing host and bacterial proteins. The CCV membrane itself serves as a barrier to protect the bacteria from the host's innate immune response, and the lipid and protein content directly influence both the CCV luminal environment and interactions between the CCV and host trafficking pathways. CCV membrane cholesterol is critical in regulating CCV pH, while CCV phosphatidylinositol phosphate species influence CCV fusion events and membrane dynamics. C. burnetii proteins directly target host lipid metabolism to regulate CCV membrane content and generate a source of lipids that support bacterial replication or influence the innate immune response. This review provides an overview of the diverse repertoire of lipids involved in CCV formation and maintenance, highlighting the pathogen-driven strategies to modify host lipid homeostasis.