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Clinical and Diagnostic Laboratory Immunology, May 2002, p. 616-621, Vol. 9, No. 3
1071-412X/02/$04.00+0 DOI: 10.1128/CDLI.9.3.616-621.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.
HIV Immunology and Diagnostics Branch, Division of AIDS, STD, and TB Laboratory Research,1 Investigation and Prevention Branch, Hospital Infections Program, National Center for Infectious Diseases,2 Office of Global Health,3 Division of Laboratory Sciences, National Center for Environmental Health, Centers for Disease Control and Prevention, U.S. Department of Health and Human Services, U.S. Public Health Service, Atlanta, Georgia 30333,4 Lilongwe Central Hospital and the Community Health Sciences Unit, Ministry of Health and Population, Lilongwe, Malawi5
Received 1 August 2001/ Returned for modification 5 November 2001/ Accepted 26 January 2002
In animal studies, vitamin A deficiency induces a shift from type 2 (humoral) to type 1 (cellular) cytokines; there are no similar data for humans. Control of human immunodeficiency virus (HIV) and Mycobacterium tuberculosis infections requires type 1 cytokine (cellular) immunity. These infections and vitamin A deficiency are highly prevalent in Africa. We therefore examined the interactions among serum vitamin A levels, immune parameters, HIV infection status, Mycobacterium bovis BCG vaccine scarring (as an indicator of a type 1 cytokine profile), and clinical findings for 70 hospitalized children in Malawi, Africa. Directly conjugated monoclonal antibodies and flow cytometry were used to assess cell-specific cytokine production by peripheral blood monocytes and lymphocyte subpopulations. The statistical techniques employed included nonparametric statistics and logistic regression analyses. Thirty percent of the participants had severe vitamin A deficiency (<10 µg/dl), 34% had moderate deficiency (10 to <20 µg/dl), and 36% had normal levels (
20 µg/dl). Vitamin A levels were lower for HIV-positive than for HIV-negative children (median, 10 and 17 µg/dl, respectively). Vitamin A-deficient children (<20 µg/dl) were more likely than non-vitamin A-deficient children to have higher proportions of natural killer (NK) cells (median, 8.3 and 5.2%, respectively) and lower ratios of interleukin-10-producing monocytes to tumor necrosis factor alpha-producing monocytes after induction (median, 1.0 and 2.3, respectively). Vitamin A-deficient children were also more likely than non-vitamin A-deficient children to exhibit respiratory symptoms (47% versus 12%) and visible BCG vaccine scars (83% versus 48%), which are indicative of a type 1 response to vaccination. Vitamin A status did not vary with gender, age, incidence of malaria parasitemia, blood culture positivity, or rates of mortality (6% of vitamin A-deficient children died versus 20% of non-vitamin A-deficient children). Lower vitamin A levels were associated with a relative type 1 cytokine dominance and proportionately more NK cells, both of which may be somewhat beneficial to persons who are exposed to HIV, M. tuberculosis, or other type 1 pathogens.
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