However, and to our surprise, the ablation of IFNαβR from normal memory T cells prior to the secondary viral infection did not prevent this attrition, indicating that an alternative pathway(s) must be contribute to the process; we speculate that this may be driven by CD8+ T cell derived IFNγ, which is produced in the hours immediately following secondary viral infection (Fig 1) [35]. Here, IFNAR2 is linked to viral infectious disease.