Specifically, we demonstrate that IFNAR and not PD-L1 is required for the accumulation of virus-specific CD8+ T cells to prevent virus persistence and chronic LCMV-Arm infection, whereas in the absence of IFN-I signalling, PD-L1 is required to prevent an overexuberant CD8+ T cell response from causing severe lung damage and mortality. The gene discussed is IFNAR1; the disease is infection.