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CTL immune responses play a central role in the control of viral replication as it has been observed in Long Term Non-Progressor (LTNP) patients. Different mechanisms for viral inhibition mediated by CTL immune response have been observed. HIV infected cells are recognized by the TCR of HIV-specific CTLs when viral peptides are presented at the cell surface in the context of HLA class?I?molecules. This recognition leads to CTL cytotoxic immune response[7]. Humoral immune response has a secondary role in the control of HIV infection. Although neutralizing antibodies reduce the virus particles and therefore the viral spread. However, serum of the infected patients does not reduce the viral infectivity in vitro and the efficacy of gp120 neutralizing antibodies is reduced. This is due to the fact that gp120, HIV glycoprotein responsible for diglyceride the viral entry, has a high mutation frequency which leads to conformational changes impairing the antibody binding[7]. Due to the lack of capability of the immune response to eradicate HIV, the infection becomes chronic and the virus is integrated in a latent form in the human genome. Despite the return of circulating CD4+T cells to normal levels, massive immune activation and accelerated cell turnover takes place. The ultimate consequence of immune activation is the see more depletion of CD4+ T cells. In absence of T helper response the immune system is not able to control other infections, therefore opportunistic infections occur and lead to AIDS[1]. In general, HIV protective immune response is associated with recognition and activation of the cytolytic function exerted mostly by NK and CD8+ T cells. Thus, the contribution of HLA molecules and its ligands play a key role in controlling HIV disease progression[8]. HIV PROGRESSION The progression of HIV infection has different phases. In the primary infection, HIV infects mainly macrophages and dendritic cells by using the co-receptor C-C chemokine receptor 5 (CCR5) together with the selleck chemical CD4 molecule. Virus replication in the lymph nodes leads to the viremic peak characteristic of acute infection[4,5]. The viremia increases the viral spread in the other lymph nodes of the entire organism. The immune system mounts a response to control the viremia, which decreases towards a stationary phase named ��set point��. In most of the cases, the immune response is not capable to eradicate the infection. Therefore, an equilibrium between host and virus occurs and the viral DNA is integrated in a latent form that could not be detected by the immune system[6]. In the late phase of the infection, the constant viral replication induces a tropism shift. The virus prefers C-X-C chemokine receptor type 4 co-receptor (CXCR4) and infects mainly the CD4+ T-cells. The CD4+ T-cells depletion (