Model summarizing the Tax-1–G-protein interactions. After T-cell infection by HTLV-1, Tax-1 induced the expression of several genes, including chemokines, that bound to their specific GPCRs. Tax-1 also migrated to the cytoplasm and the plasma membrane, bound to the Gβγ heterodimer complex, and regulated specific ligand-receptor interaction, T-cell migration, and intracellular G-protein effector activation. Tax-1 also affected intracellular Gβγ-effector activation by direct binding to the Gβ subunit and by inactivating the G-protein pathway suppressor 2. As a feedback loop, Gβγ inhibits HTLV-1 expression and contributes to viral escape from immune surveillance.