Enhanced proliferation of HIV causes immune responses that attempt to eliminate the virus. So, HIV maintains a latent infection in order to survive within the host. The Vpu protein suppresses NF-κB activation by inhibition of proteasome-dependent degradation of IκB [24] . The Nef protein suppresses phosphorylation of ERK through induction of a phosphatase MKP-1 [25] . This causes suppression of TNF-α production by macrophages via TLR4 signaling. Because TNF-α is necessary for maturation and translocation of DCs (including Langerhans cells) to the lymph nodes, downregulation of TNF-α leads to suppression of acquired immune responses, and so prevents inhibition of virus proliferation by activated T lymphoctes. Furthermore, Nef inhibits T cell receptor induced lymphocyte activation [26] . These strategies contribute to the suppression of HIV proliferation in the lymph nodes, and also inhibit the propagation of infection. Other immunosuppressive mechanisms used by HIV have also been reported. Cosuppressive molecules, such as B7-H1 on DCs and PD1 on T lymphocytes, are upregulated in patients with HIV, and induce apoptosis through their interaction with DCs and T lymphocytes. In addition, HIV is thought to induce regulatory T cells [27] .