Autophagy is a catabolic process used for the degradation of cytoplasmic organelles and proteins. Macroautophagy involves the formation of autophagosomes and subsequent fusion with a lysosome to mediate cargo degradation. Autophagy is also used as a cellular defence mechanism during viral infection. Previous studies have shown that different viruses can interact and manipulate the autophagic pathway of the host cell to assure successful replication and virion assembly.
For vaccinia virus (VACV), the prototypic poxvirus, it has been demonstrated that the double membrane vesicle formed during autophagy do not serve as the source of the mature virion membrane. On the other hand, it was found that VACV infection causes LC3 lipidation and abrogation of autophagy, the virus can prevent autophagosome formation. We hypothesize that VACV encodes a factor to counteract host autophagy during replication of the virus to avoid autophagic degradation of the viral proteins. The aim of my PhD project is to determine how VACV modulates host cell autophagy and to investigate the viral factors involved in this process.
2015 | Master of Science in Life and Medical Science, University of Bonn, Germany
2012 | Bachelor of Science in Cell Biology, University of Osnabrueck, Germany
2018 | Associate Fellow of the Higher Education Academy
2015 | MRC PhD Stipend
2012 | RISE scholarship, German Academic Exchange Service (DAAD)
2011 | RISE scholarship, German Academic Exchange Service (DAAD)
2009 | Karl von Frisch Award, Society of German Biologists (VBIO)
Medical Research Council
Viral pathogens, Signalling pathways, Autophagy
Light microscopy, High throughput screening, Biochemistry