Autophagy is a catabolic process used for the degradation of organelles and proteins. Macroautophagy involves the formation of autophagosomes and subsequent fusion with a lysosome to mediate cargo degradation. It also functions as a cellular defence mechanism during viral infection known as xenophagy. Previous studies have shown that different viruses can manipulate the autophagy pathway of the host cell to assure successful replication and virion assembly. 

Vaccinia virus (VACV), the prototypic poxvirus, replicates exclusively in the cytoplasm of its host. It has been demonstrated that the double membrane vesicles formed during autophagy do not serve as the source of the mature virion membrane. However, it was also found that VACV infection causes LC3 lipidation and prevents autophagosome formation. We hypothesize that VACV encodes a set of proteins to counteract host autophagy on multiple layers during viral replication. Thus VACV avoids degradation of viral proteins produced during virion assembly. The aim of my project is to determine how VACV modulates host cell autophagy and to investigate the viral and cellular factors involved in this process.