**1. Introduction**

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HIV infection has been associated with a high oxidative stress profile. Different stages of the infection are marked with distinct characteristics of redox activity culminating to either potentiation of the disease or an ameliorative process. Both host and viral survival rates require varying degrees of antioxidants to counter the devastating effect of oxidative stress (OS) molecules produced during the onset of the infection. Here, the chapter x-rays and brings to concept the oxidative stress condition and its implication on HIV functional cure. It is obvious that 'excess' free radicals could destroy cell membranes and generate apoptosis, the main cause of lymphocyte-CD4+ depletion in HIV infection. The whole scenario demonstrates that measurement of oxidative stress molecule could function as a potentially HIV biomarker and surveillance parameter in addition to CD4 cell count and that its regulation controls the HIV infection processes.

Generally, people with HIV infection have an unbalanced redox system which is related to a depletion of protective system (glutathione peroxidase; superoxide dismutase; vitamins A, C and E; selenium; etc.), activation of immune signalling molecules (cytokines and chemokines) and an increased production of free radicals (superoxide anion, hydrogen peroxide and hydroxyl radicals). Immunological and biological consequences of this condition include activation of lymphocytes and phagocytising cells, chronic inflammation, increased polyun‐ saturated fatty acid concentration and lipoperoxidation and direct or indirect effect of several pathologic agents. As the search for HIV functional cure intensifies, oxidative stress condition of natural controllers of HIV infection remains an integral success path for a possible disease cure and management.

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