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Results We have demonstrated that, through a regular IFN-a signal transduction pathway, IFN-a can significantly enhance the expression of APOBEC3G in human primary resting but not activated CD4 T-cells, and the amounts of APOBEC3G associated with a low molecular mass (LMM). Interestingly, short-time treatments of newlyinfected resting CD4 T-cells with IFN-a will significantly inactivate human immunodeficiency virus type 1 (HIV-1) at its early stage. This inhibition can be counteracted by APOBEC3G-specific short interfering RNA (siRNA), indicating that IFN-a-induced APOBEC3G plays a key role to mediate this anti-HIV-1 process.

Up-regulation of interferon-a/APOBEC3G signal pathway potently inactivates HIV-1 infectivity in resting CD4-T cells