Speaker
Description
Coxiella burnetii is the causative agent of the zoonotic disease Q fever. Aside from acute fever, few patients can develop chronic Q fever months or years after primary infection, mainly characterized as endocarditis. 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, 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. This suggests that under hypoxia, C. burnetii might undergo stringent response or enters the metabolically inactive small cell-variant form (SCV) to survive nutritional limitation. To characterize C. burnetii under these conditions we infected primary murine macrophages with C. burnetii under normoxic and hypoxic conditions and analyse 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. drug sensitivity will be analysed.
Keywords
C. burnetii, hypoxia, small cell variant and persistence
| Junior Scientist Status | Yes, I am a Junior Scientist. |
|---|---|
| Professional Status of the Speaker | PhD Student |
| Registration-ID code | #477 |
Primary author
Co-authors
External references
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