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Abstract

Previous research in our lab described that dengue virus induces a lipid droplet (LD) specific autophagy program (lipophagy) that benefits viral replication by increasing b-oxidation of free fatty acids, presumably for increased ATP and energetic intermediates. However, it was unclear how dengue virus triggered this process. In this thesis, I show i) that lipophagy depends on a TGFβ-TAK1-AMPK-mTORC1-dependent signaling cascade; ii) LDs are targeted for degradation in an ubiquitin- and NBR1-dependent fashion; and iii) that NS1-3 is sufficient for lipophagy induction.

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