Role of ER stress in SARS-CoV-2 lung infection (A04)

• Subject Area: Parasitology and Biology of Tropical Infectious Disease Pathogens
• Term: from 2010 to 2023
• Project identifier: Deutsche Forschungsgemeinschaft (DFG) - Project number 114933180

Viral infections may trigger ER stress activating the UPR signaling and MAPK pathways. Both pathways may impact on innate immune activation and cell fate decision. Our unpublished data indicate UPR activation in SARS-CoV-2 infected human lung tissue. We hypothesise that SARS-CoV- 2 activates UPR and MAPK signaling thereby modulating viral-host interaction and immune response. We will investigate the ability of determinant SARS-CoV-2 components to induce UPR response in SARS-CoV-2 infection. We will deploy the versatile SNAP-tag to produce labeled surface SARS-CoV- 2 proteins in lung cells as well as 3D models and investigate their capability to induce transient shutdown on protein translation and allow determination of intracellular localization. We will provide bacterial SARS-CoV-2 S1 containing bacterial membrane vesicles (BMVs) for vaccination studies in the CRC-TR84.

• DFG Programme: CRC/Transregios
• Subproject of: TRR 84: Innate Immunity of the Lung: Mechanisms of Pathogen Attack and Host Defence in Pneumonia
• Applicant Institution: shared FU Berlin and HU Berlin through:; Charité - Universitätsmedizin Berlin
• Project Heads: Privatdozent Dr. Mobarak Abu Mraheil, since 11/2018; Professor Dr. Trinad Chakraborty; Professor Dr. Stefan Hippenstiel, since 7/2018; Dr. Helena Pillich, from 7/2018 until 11/2018