Influenza virus repurposes the antiviral protein IFIT2 to promote translation of viral mRNAs

• Published in: Nature microbiology Vol. 5; no. 12; pp. 1490 - 1503
• Main Authors: Tran, Vy, Ledwith, Mitchell P., Thamamongood, Thiprampai, Higgins, Christina A., Tripathi, Shashank, Chang, Max W., Benner, Christopher, García-Sastre, Adolfo, Schwemmle, Martin, Boon, Adrianus C. M., Diamond, Michael S., Mehle, Andrew
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 01.12.2020; Nature Publishing Group
• Subjects: 13; 13/1; 13/106; 13/109; 38/39; 38/47; 38/91; 45; 45/29; 45/41; 45/70; 59; 631/326/596/1578; 631/326/596/2557; 631/337/574; 631/337/574/1789; 64; 692/699/255/1578; 82; 82/80; 82/83; 96; Animals; Antiviral activity; Apoptosis Regulatory Proteins - genetics; Apoptosis Regulatory Proteins - immunology; Biomedical and Life Sciences; Cell death; Cell Line; CRISPR; Enhancers; Gene expression; Host-Pathogen Interactions; Humans; Infectious Diseases; Influenza; Influenza A virus - genetics; Influenza A virus - physiology; Influenza, Human - genetics; Influenza, Human - immunology; Influenza, Human - virology; Interferon; Life Sciences; Medical Microbiology; Mice; Mice, Knockout; Microbiology; Parasitology; Protein Biosynthesis; Proteins; Replication; RNA, Messenger - genetics; RNA, Messenger - metabolism; RNA, Viral - genetics; RNA, Viral - metabolism; RNA-Binding Proteins - genetics; RNA-Binding Proteins - immunology; Translation; Virology; Virus Replication

Cells infected by influenza virus mount a large-scale antiviral response and most cells ultimately initiate cell-death pathways in an attempt to suppress viral replication. We performed a CRISPR–Cas9-knockout selection designed to identify host factors required for replication after viral entry. We...