Viral suppression of cellular antiviral responses

Virus infection triggers several innate antiviral responses like the type I IFN and stress response pathway. Activation of the stress response pathway leads to inhibition of cellular translation and the formation of stress granules (SG), which have been proposed to function as a platform for viral RNA recognition. In addition, virus infection can turn on autophagy pathways and lead to changes in cellular metabolism. Most viruses have developed mechanisms to suppress IFN and stress response pathways and to redirect autophagy pathways and cellular metabolism for their own benefit. The aim of this study is to gain more insight how specific proteins of picornaviruses (e.g. enterovirus, kobuvirus and FMDV)- and coronaviruses, including SARS-CoV-2,  antagonize IFN and stress response pathways and the proposed role of SGs in connecting these pathways. For the antagonistic mechanism, the possible role of the formation viral replication organelles (ROs) as a mean to hide viral RNA for cellular sensors will be investigated. Additionally, the role of autophagy, which has been implicated in RO formation, and metabolism changes for the viral life cycle of picorna- and coronaviruses, including SARS-CoV-2, will be evaluated.

This project is part of the One Health research program.

Chiara Aloise