IFNB1 and infection: We observed that β-arrestin 2 was ubiquitinated and degraded 12 h after infection, whereas it was deacetylated only 1 h after infection, indicating that β-arrestin 2 could normally promote the activation of IFN-β signaling and the antiviral immune response at the early stage of infection, which was decreased by virus-induced ubiquitination and degradation of β-arrestin 2 in the late stage.