The immunomodulatory effect of antioxidants in murine retrovirus-infected mice: Treatment opportunity

Abstract

The acquired immune deficiency syndrome (AIDS) is a clinical disorder caused by the human immunodeficiency virus (HIV) that induced severe immunosuppression, rendering the body highly susceptible to opportunistic infection. As HIV-infected persons survive previously life-threatening infection through the use of effective medical therapies, malnutrition has become central issues in the health care plan of long-term survivors. Nutrition is a fundamental intervention in the early and ongoing treatment of HIV disease. Nutrition therapy, in coordination with other medical interventions, can extend and improve the quality and quantity of life in individuals infected with HIV and living with AIDS. A murine AIDS (MAIDS) model, induced by LP-BM5 murine leukemia virus, has been an effective tool to investigate mechanisms of retrovirus-induced immunodeficiency. The MAIDS animal model displays a number of the features of human AIDS, including progressive lymphoproliferation and increasing severe immunodeficiency. The present studies suggested that micronutrient deficiency resulted in premature death and immune dysfunction beyond immune suppression induced by LP-BM5. Chronic EtOH consumption in murine retrovirus-infected mice caused deleterious effects on host defense, immune response, cytokine release, oxidative stress, and nutritional status. This immune dysfuction happened more severely with aging. Supplementation with antioxidants prevented retrovirus-induced suppression of immune response and prolonged the survival of retrovirus-infected mice. It maintained nearly normal cytokine production. This occurred simultaneously with restoration of tissue vitamin E and T- and B-cell proliferation. DHEAS accentuated the effects of antioxidants and maintained cytokine production, T- and B-cell proliferation, and hepatic vitamin E close to the activity level of the uninfected mice.