Crosstalk between nonstructural proteins of SARS-CoV-2 and the autophagy signaling machinery

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The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative virus of the coronavirus disease 2019 (COVID-19). Current medicinal research focuses on vaccine development and the identification of potential therapeutic targets. (Macro-)Autophagy is an intracellular degradation process responsible for the recycling of long-lived or damaged proteins and organelles. Importantly, coronavirus infection and autophagy rely on remodelling of intracellular membranes, i.e. the formation of replication organelles such as double-membrane vesicles by coronaviruses and the biogenesis of autophagosomes during autophagy. However, the involvement of autophagy-essential proteins such as components of the ULK1 complex or the class III PtdIns3K complex for the formation of SARS-CoV-2-induced double-membrane vesicles remains unclear. In this project, we aim at characterizing the crosstalk between nonstructural proteins of SARS-CoV-2 and the autophagy-inducing ULK1 and PtdIns3K complexes. Collectively, we want to identify pharmacological approaches that might point the way towards novel COVID-19 therapies.