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Coxiella burnetii is an obligate intracellular bacterium that lives in a modified lysosome termed the Coxiella containing vacuole (CCV). C. burnetii is the causative agent of the zoonotic illness Q Fever, which primarily infects ruminant livestock and can spread to humans via inhalation. Acute Q fever is characterized by a flu like illness, while chronic disease is associated with more severe symptoms including endocarditis and chronic fatigue syndrome. C. burnetii has a biphasic life cycle consisting of a small cell variant (SCV) and large cell variant (LCV). The SCV is environmentally stable and can cause infection via inhalation of 1 - 10 infectious particles. Once taken up by the host cell, C. burnetii must manipulate the signaling pathways of the host cell to form the CCV where it switches to the LCV, the metabolic and replicative form of the bacterium. It primarily accomplishes this goal by utilizing a Type IV B Secretion System (T4BSS), which is unique to C. burnetii and Legionella pneumophila. The T4BSS, along with some other secretion mechanisms, secretes effector proteins into the host cell. These proteins then interfere with or modulate the host cell to recruit vacuoles, evade detection by the immune system, and prevent the host cell from initiating apoptosis. After about 6 days, the LCV will convert to SCV and then initiate host cell lysis to spread infection. This review looked at many eukaryotic cells signaling pathways and the interactions between C. burnetii and host proteins. These interactions are responsible for the modulation of host cell pathways necessary for CCV formation and C. burnetii survival. Understanding these interactions better will help with future treatments for C. burnetii infection. Further discoveries in these interactions are crucial for the future of C. burnetii research.