Coxiella burnetii is an obligate intracellular bacterium responsible for the zoonosis Q fever. During infection, professional phagocytes internalise C. burnetii into phagosomes that develop into large vacuoles with phagolysosomal characteristics known as a parasitophorous vacuole (PV) in which C. burnetii replicates. To develop its replicative PV niche, C. burnetii delays phagolysosomal maturation by hijacking the host cells’ autophagic pathway. Many mechanisms in which C. burnetii controls its host cell processes are unknown, but it is clear that effector proteins secreted by the C. burnetii Dot/Icm Type IV B Secretion System are vital. To date, effectors have been described in playing a role in apoptosis prevention, PV formation and C. burnetii survival. To further elucidate the host cell responses to infection, and cellular processes potentially targeted by C. burnetii, we analysed the global miRNA response of THP-1 derived macrophages to C. burnetii infection. miRNA responses to other bacterial and viral infections are well characterised, but have not been determined in C. burnetii infection. During the mid-log phase growth of C. burnetii, 5 days post infection, of 1090 miRNA targets, 16 were up-regulated >3-fold (12 >4-fold) and 163 were down-regulated >3-fold (10 >4-fold) when compared to uninfected controls. To confirm the requirement of transcriptional change for some miRNAs during infection, we performed transfections which inhibited miR-3190-3p (49-fold up-regulated) and mimicked miR-7-5p (7-fold down-regulated). The transfections with the miR-7-5p mimic and the miR-101-3p mimic (a control to disrupt autophagic trafficking) both significantly decreased the intracellular growth of C. burnetii by 36% and 50% respectively, confirming their requirement for altered regulation. Further analysis of the miRNA pathways and transfection experiments will further elucidate the cellular responses to C. burnetii infection and potentially the mechanisms that C. burnetii employs to survive in its intracellular niche.