Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although a role for vitamin A in immunity to infectious diseases has long been suggested, only in the last decade have epidemiological, immunologic, and molecular studies yielded substantial evidence for a central role. The recent discovery of retinoic acid and retinoid X receptors has provided a molecular basis for the action of vitamin A and its metabolites at the level of gene activation. At least a dozen clinical trials have now demonstrated that vitamin A supplementation reduces severe morbidity and mortality from infectious diseases among children who have acute measles or who are from areas in which vitamin A deficiency is endemic. Vitamin A deficiency is an immunodeficiency disorder characterized by widespread alterations in immunity, including pathological alterations in mucosal surfaces, impaired antibody responses to challenge with protein antigens, changes in lymphocyte subpopulations, and altered T- and B-cell function. Vitamin A and its metabolites are immune enhancers that have been shown to potentiate antibody responses to T cell-dependent antigens, increase lymphocyte proliferation responses to antigens and mitogens, inhibit apoptosis, and restore the integrity and function of mucosal surfaces. Vitamin A and related retinoids may have potential applications in therapy for some infectious diseases.
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PMID:Vitamin A, immunity, and infection. 781 69

Acquired immune deficiency syndrome (AIDS) is a clinical disorder caused by a retrovirus infection and represents the end point in a progressive sequence of immunosuppressive changes. Vitamins can enhance disease resistance in animals and humans. As such they are important co-factors in optimal functioning of the immune systems. In this article, the immunological and nutritional modifications caused by AIDS are summarized. The effects of murine and human retrovirus infection on vitamin status are analyzed as co-factors in the development of severe immune dysfunction, AIDS. The properties of immunoenhancing antioxidative vitamins, vitamin A, B6, B12, C, E, and beta-carotene, which are frequently low in AIDS patients, are evaluated relative to the development of immunodeficiency during retrovirus infection. Vitamin A, E, and B12 deficiency accelerated the development of AIDS with low T cells, whereas their normalization retarded the development of immune dysfunction. The interactions between these vitamins and the immune system in human AIDS patients and animal models of AIDS are reviewed. Our purpose is to provide data on how retrovirus infection can cause nutritional deficiencies that accentuate immune damage and to evaluate the potential therapeutic role of vitamins in the treatment of immune dysfunctions in AIDS patients.
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PMID:Vitamins and immunomodulation in AIDS. 883 29

A review of recent evaluations of non-vaccine interventions for the prevention of childhood diarrhea in developing countries both confirmed the importance of standard strategies (e.g., breast feeding, water supply and sanitation improvements) and suggested refinements in approaches to personal and domestic hygiene, weaning education, and food hygiene. Despite the risk of vertical transmission of human immunodeficiency virus in infected areas, the health risks of not breast feeding far outweigh the potential number of lives saved by abandoning this practice. Weaning education programs can produce a 2-12% reduction in diarrhea mortality. Also important is the promotion of food handling, preparation, and storage practices that reduce the risk of fecal contamination. Improvements in water quantity may have a greater impact on diarrhea than improvements in quality alone through their effect on personal and domestic hygiene. Two relatively new strategies, vitamin A supplementation and prevention of low birth weight, should be promoted. Vitamin A intake is significantly associated with both all-cause and diarrhea-specific child mortality; the feasibility of large-scale supplementation programs awaits investigation of their cost-effectiveness, however. The choice of specific diarrheal control strategies depends on local factors such as diarrhea etiologies, the existing infrastructure, and government priorities. In all countries, effective implementation of preventive strategies requires the involvement of a range of sectors (e.g., health, agriculture, water supply, and sanitation).
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PMID:Prevention of diarrhoea in young children in developing countries. 918 69

Vitamin A is an essential micronutrient for normal immune function. Vitamin A deficiency is common among human immunodeficiency virus (HIV)-infected pregnant women and is associated with higher mother-to-child transmission of HIV-1 and increased infant mortality. The biological mechanisms by which vitamin A deficiency could influence mother-to-child transmission of HIV-1 include impairment of immune responses in both mother and infant, abnormal placental and vaginal pathology and increased HIV viral burden in breastmilk and blood. Clinical trials are currently in progress to determine whether daily micronutrient supplementation, including vitamin A, during pregnancy can reduce mother-to-child transmission of HIV-1.
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PMID:Overview of the potential role of vitamin A in mother-to-child transmission of HIV-1. 924 Aug 69

The use of vitamin A therapy during human immunodeficiency virus (HIV) infection is under clinical investigation, and vitamin A could potentially modulate HIV replication because the virus genome contains a retinoic acid response element. A randomized, double-masked, placebo-controlled clinical trial was conducted to determine the impact of single high-dose vitamin A supplementation, 60-mg retinol equivalent (200,000 IU), on HIV load and CD4 lymphocyte count. HIV-infected injection drug users (120) were randomly allocated to receive vitamin A or placebo. Plasma vitamin A level, CD4 lymphocyte count, and HIV load were measured at baseline and 2 and 4 weeks after treatment. Vitamin A supplementation had no significant impact on HIV load or CD4 lymphocyte count at 2 and 4 weeks after treatment. This study suggests that high-dose vitamin A supplementation does not influence HIV load.
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PMID:Vitamin A supplementation and human immunodeficiency virus load in injection drug users. 949 39

The rates of mother-to-child transmission of human immunodeficiency virus type 1 (HIV-1), progression to AIDS following HIV-1 infection, and AIDS-associated mortality are all inversely correlated with serum vitamin A levels (R. D. Semba, W. T. Caiaffa, N. M. H. Graham, S. Cohn, and D. Vlahov, J. Infect. Dis. 171:1196-1202, 1995; R. D. Semba, N. M. H. Graham, W. T. Caiaffa, J. B. Margolik, L. Clement, and D. Vlahov, Arch. Intern. Med. 153:2149-2154, 1993; R. D. Semba, P. G. Miotti, J. D. Chiphangwi, A. J. Saah, J. K. Canner, G. A. Dallabetta, and D. R. Hoover, Lancet 343:1593-1596, 1994). Here we show that physiological concentrations of vitamin A, as retinol or as its metabolite, all-trans retinoic acid, repressed HIV-1Ba-L replication in monocyte-derived macrophages (MDMs). Repression required retinoid treatment of peripheral monocytes during their in vitro differentiation into MDMs. Retinoids had no repressive effect if they were added after virus infection. Retinol, as well as all-trans retinoic acid and 9-cis retinoic acid, also repressed HIV-1 long terminal repeat (LTR)-directed expression up to 200-fold in transfected THP-1 monocytes. Analysis of HIV-1 LTR deletion mutants demonstrated that retinoids were able to repress activation of HIV-1 expression by both NF-kappaB and Tat. A cis-acting sequence required for retinoid-mediated repression of HIV-1 transcription was localized between nucleotides -51 and +12 of the HIV-1 LTR within the core promoter. Protein-DNA cross-linking experiments identified four proteins specific to retinoid-treated cells that bound to the core promoter. We conclude that retinoids render macrophages resistant to virus replication by modulating the interaction of cellular transcription factors with the viral core promoter.
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PMID:Retinoid-induced repression of human immunodeficiency virus type 1 core promoter activity inhibits virus replication. 962 Oct 47

Vitamin A levels in plasma and other nutritional indices were measured during pregnancy for 449 women enrolled in a multicenter cohort study of mother-to-infant transmission of human immunodeficiency virus type 1 (HIV-1). During the third trimester, 29.6% of the women had low (20 to <30 microg/dL) and 11.1% had very low (<20 microg/dL) vitamin A levels. Vitamin A and body mass index, serum albumin levels, and hemoglobin levels were weakly correlated. After adjustment for other covariates, women with low and very low vitamin A levels before the third trimester were more likely to deliver infants with low birth weight (<2500 g) than were those with higher levels (odds ratio [OR], 4.58; 95% confidence interval [CI], 1.57-13.4; and OR, 6.99; 95% CI, 1.09-45.0, respectively). However, there was no statistically significant association between vitamin A level and mother-to-infant transmission of HIV-1. Anemia and low body mass index before the third trimester were associated with an increased risk of transmission in univariate analyses but not in multivariate analyses.
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PMID:Vitamin A deficiency and other nutritional indices during pregnancy in human immunodeficiency virus infection: prevalence, clinical correlates, and outcome. Women and Infants Transmission Study Group. 1047 37

Vitamin A administered to children infected with the human immunodeficiency virus before influenza vaccination in a double-blind randomized study did not enhance vaccine serologic responses but did dampen the increase in the human immunodeficiency virus viral load 14 days after immunization (vitamin A, decrease of 0.13 +/- 0.09 log(10) copies/mL; placebo, increase of 0.14 +/- 0.08, P =.02).
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PMID:Effect of vitamin A therapy on serologic responses and viral load changes after influenza vaccination in children infected with the human immunodeficiency virus. 1075 59

Breast milk vitamin A is not well characterized as an indicator of vitamin A status in women with infections. A controlled trial of vitamin A, 3 mg retinol equivalent/day, was conducted among 697 pregnant women with human immunodeficiency virus (HIV) infection in Malawi which allowed comparison of plasma versus breast milk vitamin A as indicators of vitamin A status. Retinol concentrations were measured in plasma at baseline (18-28 weeks) and 38 weeks gestation and breast milk at 6 weeks post-partum. Plasma alpha 1-acid glycoprotein (AGP) and C-reactive protein (CRP) were measured at baseline. Plasma retinol (geometric mean, SD) at 38 weeks was 0.72 (0.44, 1.18) and 0.61 (0.38, 0.98) mumol/L (P < 0.0002) and breast milk retinol was 1.32 (0.71, 2.43) and 0.95 (0.49, 1.82) mumol/L (P < 0.0001) in vitamin A and placebo groups, respectively. Women with elevated acute phase protein (AGP > 1 gm/L and/or CRP > 5 mg/L) at baseline who received vitamin A had significantly higher plasma and breast milk vitamin A at follow-up compared with placebo. Elevated acute phase proteins did not distinguish women with low body stores of vitamin A. Breast milk retinol appears to be a better indicator of vitamin A status than plasma retinol in women with infections.
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PMID:Plasma and breast milk vitamin A as indicators of vitamin A status in pregnant women. 1121 51

The associations of hemoglobin, hematocrit, and packed cell volume with socioeconomic factors, malaria, human immunodeficiency virus (HIV) infection, and nutritional status were examined among 687 children admitted to hospital with pneumonia participating in a double blind, placebo-controlled trial of vitamin A supplementation. Children were randomized to receive 2 doses of vitamin A (200,000 IU) or placebo at baseline, and additional doses at 4 and 8 months after discharge from hospital. Hemoglobin levels were measured at enrollment and, on a subset of 161 children, during follow-up. At baseline, hemoglobin concentration was positively associated with the number of possessions in the household, maternal level of education and quality of water supply, and inversely related to malaria infection after controlling for potential confounding variables. Children infected with HIV experienced a significant fall in mean hemoglobin levels over time. The risk of developing severe anemia (< 7 g/dL) during follow-up was lower for children who were breastfed for longer than 18 months as compared to those with less than 6 months of breastfeeding (adjusted prevalence ratio = 0.14, 95% confidence interval [CI] = 0.02, 0.93; P = 0.04), and higher for children over two years of age as compared to 6 to 11 months-old infants (adjusted prevalence ratio = 8.11, 95% CI = 1.2, 55.8; P = 0.03). Children with repeated diagnoses of malaria had 4.1 times the risk of developing severe anemia than did children without the diagnosis (95% CI = 1.3, 13.5; P = 0.02). Vitamin A supplements were associated with an overall nonsignificant reduction of 14% in the risk of developing severe anemia (adjusted prevalence ratio = 0.86, 95% CI = 0.37, 1.99; P = 0.73). We conclude that malaria, HIV infection, low socioeconomic status, and short duration of breastfeeding are strong and independent determinants of adverse hematologic profiles in this population.
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PMID:Vitamin A supplementation and other predictors of anemia among children from Dar Es Salaam, Tanzania. 1128 70


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