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SARS-CoV-2 shifts transcription of host gene to increase Spike acylation and boost infectivity | |
Béatrice Kunz Audrey Chuat Francisco Mesquita laurence ABRAMI lucie bracq Nattawadee Panyain Vincent Mercier Joana Carlevaro-Fita didier trono Gisou van der Goot | |
Acceso Abierto | |
Atribución-NoComercial-SinDerivadas | |
https://doi.org/10.1101/2023.04.15.537011 | |
https://www.biorxiv.org/content/10.1101/2023.04.15.537011v1 | |
ABSTRACT SARS-CoV-2 infection requires Spike protein mediating fusion between the viral and cellular membranes. The fusogenic activity of Spike requires its post-translational lipid modification by host S-acyltransferases, predominantly ZDHHC20. Previous observations indicate that SARS-CoV-2 infection augments the S-acylation of Spike when compared to transfection. Here, we find that SARS-CoV-2 infection triggers a change in the transcriptional start site of the zddhc20 gene, both in cells and in an in vivo infection model, resulting in a 67-amino–acid-long N-terminally extended protein with 37-times higher Spike acylating activity, leading to enhanced viral infectivity. Furthermore, we observed the same induced transcriptional change in response to other challenges, such as chemically induced colitis, indicating that SARS-CoV-2 hijacks an existing cell damage response pathway to generate more infectious viruses. | |
bioRxiv | |
17-04-2023 | |
Preimpreso | |
Inglés | |
Público en general | |
VIRUS RESPIRATORIOS | |
Aparece en las colecciones: | Materiales de Consulta y Comunicados Técnicos |
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