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Programmed Ribosomal Frameshifting Activates GCN2 to Suppress Host Translation and Boost RNA Virus Replication

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Programmed ribosomal frameshifting acts as a regulatory stress signal that activates GCN2 and shuts down host translation. A minimal SARS‑CoV‑2 frameshift element triggers this response independently of ZAKα and is required for viral propagation. DRG1 and IGF2BP3 mediate GCN2 activation, and the mechanism extends to HIV‑1 and West Nile virus.



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Programmed ribosomal frameshifting triggers GCN2 to shut host translation and enhance replication in multiple RNA viruses.

 
 
 

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