HIV establishes a latent infection in resting T lymphocyte, and T lymphocyte activation by DCs or stimulation with IL-2 is thought to trigger active replication of the virus. Resting T lymphocytes show resistance to infection and proliferation of HIV. Apolipoprotein B mRNA editing enzyme catalytic polypeptide-like 3G (APOBEC3G) is important for this resistance [16, 17] . The antiviral mechanisms of APBEC3G are considered to act via inhibition of viral reverse transcriptase (RT). It also produces a transition (G to A) in the DNA strand transcribed by RT due to its cytidine deaminase activity. However, a mutant lacking cytidine deaminase retains antiviral activity. Low molecular weight complexes of APOBEC3G (LMM: 70-100 kDa) have antiviral activity, but high molecular weight complexes (HMM: 700 kDa) do not. The Vif protein of HIV converts LMM to HMM, and promotes proteasome-dependent degradation of the complex, so HIV can counteract its antiviral activity [18] . T cell activation leads to conversion of LMM to HMM (proviral environment). On the other hand, IFNs induce LMM type (antiviral environment) [19, 20] .