Mary Wilson
Well-known member
10 January 2024
https://doi.org/10.1038/s44318-023-00019-8
Evangelos D Karousis, Katharina Schubert, and Nenad Ban
Abstract
Coronaviruses are a group of related RNA viruses that cause respiratory diseases in humans and animals. Understanding the mechanisms of translation regulation during coronaviral infections is critical for developing antiviral therapies and preventing viral spread. Translation of the viral single-stranded RNA genome in the host cell cytoplasm is an essential step in the life cycle of coronaviruses, which affects the cellular mRNA translation landscape in many ways. Here we discuss various viral strategies of translation control, including how members of the Betacoronavirus genus shut down host cell translation and suppress host innate immune functions, as well as the role of the viral non-structural protein 1 (Nsp1) in the process. We also outline the fate of viral RNA, considering stress response mechanisms triggered in infected cells, and describe how unique viral RNA features contribute to programmed ribosomal −1 frameshifting, RNA editing, and translation shutdown evasion.
https://www.embopress.org/doi/full/10.1038/s44318-023-00019-8
https://doi.org/10.1038/s44318-023-00019-8
Evangelos D Karousis, Katharina Schubert, and Nenad Ban
Abstract
Coronaviruses are a group of related RNA viruses that cause respiratory diseases in humans and animals. Understanding the mechanisms of translation regulation during coronaviral infections is critical for developing antiviral therapies and preventing viral spread. Translation of the viral single-stranded RNA genome in the host cell cytoplasm is an essential step in the life cycle of coronaviruses, which affects the cellular mRNA translation landscape in many ways. Here we discuss various viral strategies of translation control, including how members of the Betacoronavirus genus shut down host cell translation and suppress host innate immune functions, as well as the role of the viral non-structural protein 1 (Nsp1) in the process. We also outline the fate of viral RNA, considering stress response mechanisms triggered in infected cells, and describe how unique viral RNA features contribute to programmed ribosomal −1 frameshifting, RNA editing, and translation shutdown evasion.
https://www.embopress.org/doi/full/10.1038/s44318-023-00019-8