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dc.contributor.advisorWatson, Ronald R.en_US
dc.contributor.authorLee, Jeongmin
dc.creatorLee, Jeongminen_US
dc.date.accessioned2013-04-25T09:54:58Zen
dc.date.available2013-04-25T09:54:58Zen
dc.date.issued1999en_US
dc.identifier.urihttp://hdl.handle.net/10150/284082en
dc.description.abstractThe 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.
dc.language.isoen_USen_US
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en_US
dc.subjectHealth Sciences, Nutrition.en_US
dc.subjectHealth Sciences, Immunology.en_US
dc.titleThe immunomodulatory effect of antioxidants in murine retrovirus-infected mice: Treatment opportunityen_US
dc.typetexten_US
dc.typeDissertation-Reproduction (electronic)en_US
thesis.degree.grantorUniversity of Arizonaen_US
thesis.degree.leveldoctoralen_US
dc.contributor.committeememberWatson, Ronald R.en_US
dc.contributor.committeememberBernstein, Harrisen_US
dc.contributor.committeememberLarson, Douglas F.en_US
dc.identifier.proquest9960293en_US
thesis.degree.disciplineGraduate Collegeen_US
thesis.degree.disciplineNutritional Sciencesen_US
thesis.degree.namePh.D.en_US
dc.identifier.bibrecord.b4027391xen_US
refterms.dateFOA2018-09-06T00:45:45Z
html.description.abstractThe 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.


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