Bclaf1 critically regulates the type I interferon response and is degraded by alphaherpesvirus US3

• DOI: 10.1371/journal.ppat.1007559
• Publication Date: 2019-01-25T18:58:32Z
• Authors: Chao Qin; Rui Zhang; Yue Lang; Anwen Shao; Aotian Xu; Wenhai Feng; Jun Han; Mengdong Wang; Wanwei He; Cuilian Yu; Jun Tang
• Keywords: STAT2; STAT1; Transcription; IRF1

Type I interferon response plays a prominent role against viral infection, which is frequently disrupted by viruses. Here, we report Bcl-2 associated transcription factor 1 (Bclaf1) degraded during the alphaherpesvirus Pseudorabies virus (PRV) and Herpes simplex type (HSV-1) infections through protein US3. We further reveal that Bclaf1 functions critically in signaling. Knockdown or knockout of cells significantly impairs interferon-α (IFNα) -mediated gene inhibition US3 deficient PRV HSV-1. Mechanistically, maintains mechanism allowing STAT1 STAT2 to be efficiently phosphorylated IFNα, more importantly, facilitates IFN-stimulated 3 (ISGF3) binding with elements (ISRE) for efficient directly interacting ISRE STAT2. Our studies establish importance IFNα-induced antiviral immunity control infections.