Abstract
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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