Viral N protein hijacks deaminase-containing RNA granules to enhance SARS-CoV-2 mutagenesis

ABSTRACT: Host cell-encoded deaminases act as antiviral restriction factors to impair viral replication and production through introducing mutations in the viral genome. We sought to understand whether deaminases are involved in SARS-CoV-2 mutation and replication, and how the viral factors interact with deaminases to trigger these processes. Here, we show that APOBEC and ADAR deaminases act as the driving forces for SARS-CoV-2 mutagenesis, thereby blocking viral infection and production. Mechanistically, SARS-CoV-2 nucleocapsid (N) protein, which is responsible for packaging viral genomic RNA, interacts with host deaminases and colocalizes with them at stress granules to facilitate viral RNA mutagenesis. N proteins from several coronaviruses interact with host deaminases at RNA granules in a manner

SUBMITTER: Dr. Zhean Li 

PROVIDER: S-SCDT-10_1038-S44318-024-00314-Y | biostudies-other |

REPOSITORIES: biostudies-other