Coxiella burnetii is an obligate intracellular bacterium that causes Q fever in both humans and domestic ruminants. Humans get infected by inhalation of contaminated aerosols from infected ruminants. Almost 95% of cases are either asymptomatic or present as mild flu-like illness, pneumonia or hepatitis. However, 3-5% cases can develop chronic Q fever months or years after primary infection. The clinical picture of chronic Q fever suggests that C. burnetii establishes a persistent state. Yet, information about the induction of persistence is rare. STAT3 is important for host immunity and controls the expression of citrate transporter and citrate synthase. Under hypoxic conditions (0.5% O2), stabilization of HIF1a impairs the STAT3 activity, resulting in reduction of the TCA cycle intermediate citrate. Citrate limitation results in inhibition of C. burnetii replication without interfering with the viability of the pathogen. Here, we aim to characterize hypoxia-induced persistence of C. burnetii, to clarify whether C. burnetii might undergo stringent response or enters the metabolically inactive small cell-variant form (SCV) to survive this environmental stress condition. Thus, we infected primary murine macrophages with C. burnetii under normoxic (21% O2) and hypoxic (0.5% O2) conditions and analysed the expression of stringent response and SCV genes. Our data suggests that C. burnetii does not undergo stringent response, but instead enters the SCV as non-replicating persistent form. Further research is required to validate this assumption. For this bacterial morphology, bacterial ability to invade new target cells and to withstand adverse conditions, e.g. antibiotic treatment will be analysed.