In its latest report, the Joint United Nations Program on HIV/AIDS (2016) estimated that there were 36.5 million people living with HIV/AIDS in 2015, compared to 26.2 million in 1999, increasing by 41% the number of infected. Africa accounts for 69% of all cases. Other continents are also of concern, with 5 million infected in Asia, 1.5 million in North America, 1.4 million in Eastern Europe and 1.4 million in Latin America. HIV infection is characterized by the coexistence of immunodeficiency, driven by infection and depletion of CD4 + cells and chronic systemic activation of innate and adaptive immunity. HIV-infected individuals have a higher risk of developing specific types of cancer when compared to the general population, particularly Kaposi's sarcoma, non-Hodgkin's lymphoma, and invasive cervical carcinoma that are classified as AIDS-defining cancers. DNA repair is a key defense mechanism for maintaining genome integrity, repairing damage from exposure to environmental xenobiotics, as well as endogenous damage (eg from oxidative metabolism) or the spontaneous disintegration of chemical bonds in the genome, preventing the appearance of cancer. There is a need to individually and combined evaluate the influence of defective repair genes on HIV/AIDS patients and the impact of these defective genes on genetic stability and susceptibility to cancer.

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The NCR receptors play a fundamental role in the cytotoxicity mediated by NK cells against tumor cells. In the current study, we investigated possible HIV/AIDS-related changes in the expression of the NCR receptors comparing healthy donors, HIV/AIDS patients, and HIV/AIDS patients with cancer (HIV/AIDSWC). The NCRs were quantified in NK cells (NKdim and NKbright) and T lymphocytes from peripheral blood samples by flow cytometry. We found a significant decrease in the frequency of NK cells expressing NKp46 in HIV/AIDS group (p = 0.0012). There was a decrease in the frequency of NK cells expressing NKp46 in the HIV/AIDSWC group; however, this was not statistically significant. We found a significant decrease in the frequency of NK cells expressing NKp30 in the HIV/AIDS group (p = 0.0144). There was a decrease in the frequency of NK cells expressing NKp30 and in the HIV/AIDSWC group, but this was not statistically significant. There were no changes in the distribution of NK cells and their subtypes in both groups.

examined in the total NK cell population and CD56dim and CD56bright NK cell subsets separately and Tand NKT-cell populations. There was a significant increase of the expression of NKG2D (CD134) in T lymphocytes in HIV/AIDS and HIV/AIDSWC compared to healthy donors. There were no significant changes of this receptor in NK cells (and their subtypes) and NKT to compare them with healthy donors.As for the CD94 receptor, there were no significant changes of this receptor on NK cells (and their subtypes), NKT cells and T Lymphocyte to compare them with healthy donors, except for the increase in percentage of the expression in CD56bright cells, however this was not true in absolute terms.