IFNa is produced in large amounts during the acute phase of many viral infections [3, 4, 5, 6] . Direct activation of interferonstimulated genes enhances naïve T-cell survival through increased Bcl-2 and reduced Bax activation [7] and contributes to clonal expansion of antigen-specific T-cells [8] . Recent data suggest that early therapeutic intervention with pegylated IFNa rescues polyfunctional memory T-cells expressing high levels of the IL-7 receptor alpha chain (CD127) and Bcl-2, allowing a higher rate of sustained viral response [9] . However, despite good efficacy, IFNa-based therapies lead to sustained anemia, thrombocytopenia, neutropenia and lymphocytopenia [10, 11, 12, 13, 14] . Moreover, pegylated IFNa therapy enhances the risk of infection in older HCV-infected patients and HIV-infected individuals, independently from neutropenia [15, 16, 17] .