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)

Breast milk samples from human immunodeficiency virus type 1 (HIV-1)-seropositive women were analyzed by polymerase chain reaction to determine the prevalence and determinants of HIV-1-infected cells in breast milk. Breast milk samples (212) were collected from 107 women, and 58% of the samples had detectable HIV-1 DNA. The proportion of HIV-1-infected cells in the milk samples ranged from 1 to 3255/10(4) cells. Breast milk samples with detectable HIV-1 DNA were more likely to be from women with absolute CD4 cell counts of < 400 (odds ratio, 3.1; 95% confidence interval [CI], 1.5-7.0). Severe vitamin A deficiency (< 20 micrograms/dL) was associated with a 20-fold increased risk of having HIV-1 DNA in breast milk among women with < 400 CD4 cells/mm3 (95% CI, 2.1-188.5). Women with CD4 cell depletion, especially those with vitamin A deficiency, may be at increased risk of transmitting HIV-1 to their infants through breast milk.
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PMID:Human immunodeficiency virus type 1-infected cells in breast milk: association with immunosuppression and vitamin A deficiency. 759 3

Certain infections, like that with the human immunodeficiency virus-1, deplete vitamin A, and when vitamin A levels are low, immune dysfunctions establish susceptibility to further infection. Our research has focused on the immune dysfunctions that are a consequence of vitamin A deficiency and that predispose to further infection. We previously studied a helminth infection in mice, and showed that when vitamin A levels are low, the immune response develops a strong regulatory T cell imbalance with excessive T helper type-1 cell interferon (IFN)-gamma synthesis and insufficient T helper type-2 cell development and function. Here, we studied the T cell priming environment in vitamin A-deficient mice to learn how that priming environment might produce a regulatory T cell imbalance and consequently distort the ability of the immune system to respond to an infection. Our results show that during vitamin A deficiency, the priming environment included constitutive interleukin (IL)-12 and IFN-gamma transcripts, but it was devoid of constitutive IL-4 and IL-10 transcripts. Dietary all-trans-retinoic acid supplementation down-regulated the level of constitutive IL-12 and IFN-gamma transcripts. Furthermore, when T cells from naive vitamin A-deficient animals were stimulated through the T cell receptor, they produced excess IFN-gamma protein compared to T cells from control animals. In contrast, T cell stimulation failed to induce IL-4 or IL-10 secretion. The inducible IFN-gamma was largely from CD8+ T cells and all-trans-retinoic acid addition in vitro inhibited IFN-gamma production at the transcript level. Retinoic acid addition in vitro also decreased natural killer cell IFN-gamma synthesis at the transcript level. Taken together, the distorted constitutive and inducible cytokine gene expression patterns that occurred when vitamin A levels were low would be expected strongly to favor T helper type-1 development and limit T helper type-2 cell growth and differentiation, thereby limiting the animal's humoral immune response capability.
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PMID:Vitamin A deficiency results in a priming environment conducive for Th1 cell development. 761 95

A nested case-control study of vitamin A deficiency and wasting as risk factors for mortality from AIDS and infections was done within a large prospective cohort of human immunodeficiency virus (HIV)-infected injection drug users (IDUs). Fifty adult subjects who died from AIDS and infections were matched with 235 controls who survived. Plasma vitamin A, weight, and body mass index were measured. Mean length of follow-up was 2.4 +/- 1.1 years. Vitamin A deficiency occurred in 50% and wasting occurred in 38% of patients in the last visit before death. CD4 cells count < 200/microL, wasting, and vitamin A deficiency were associated with mortality. There was a higher risk of death in HIV-infected subjects with vitamin A deficiency (odds ratio [OR], 4.6; 95% confidence interval [CI], 1.8-11.3) and wasting (OR, 8.8; 95% CI, 2.7-28.2). Vitamin A deficiency and wasting are common during HIV infection and are independent predictors of mortality in HIV-infected IDUs.
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PMID:Vitamin A deficiency and wasting as predictors of mortality in human immunodeficiency virus-infected injection drug users. 856 25

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

Vitamin A deficiency severely compromises the magnitude of the primary and secondary antibody response to tetanus toxoid (TT) but does not impair the development of immunologic memory. To further characterize this immunodeficiency in antibody production, we have quantified the immunoglobulin G (IgG) subclasses (IgG1, IgG2a, IgG2b, and IgG2c) during the primary and secondary response to TT in normal, vitamin A-deficient, and retinol-repleted rats. In the primary response in normal rats, anti-TT IgG1 and IgG2b predominated. In vitamin A-deficient rats the production of anti-TT IgG2b was severely impaired, with little change in either IgG1 or IgG2a. In the secondary response vitamin A-deficient rats produced low levels of all anti-TT IgG subclasses. However, when vitamin A-deficient rats were repleted with retinol 2 days before reimmunization their secondary anti-TT IgG response was normal both in magnitude and IgG subclass distribution. This result implies that although vitamin A deficiency during the primary antibody response impaired anti-TT IgG2b production, it did not inhibit Ig heavy chain recombination or the differentiation of lymphocytes that formed memory B cells for each subclass; furthermore, these cells were activated in the secondary response after vitamin A status was improved. Thus, these experiments further support the concept that memory cell formation remains normal during vitamin A deficiency despite low levels of antibody production.
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PMID:Vitamin A status and immunoglobulin G subclasses in rats immunized with tetanus toxoid. 840 13

The maternal factors that contribute to high mortality rates among infants born to women with human immunodeficiency virus (HIV) are unclear. We followed 474 HIV-infected mothers and their infants in Malawi from pregnancy through the infants' 12th month of life. Of the 474 HIV-infected pregnant women, 300 (63.3%) were deficient in vitamin A (serum level of vitamin A, <1.05 micromol/L). Mean serum vitamin A levels among mothers whose infants died were 0.78 +/- 0.03 micromol/L compared with 1.02 +/- 0.02 micromol/L among mothers whose infants had survived for the first 12 months of life (P <.0001). The overall infant mortality rate was 28.7%. We divided HIV-positive mothers into six groups according to serum vitamin A levels (micromol/L) as follows: group 1, <0.35; group 2, between 0.35 and 0.70; group 3, between 0.70 and 1.05; group 4, between 1.05 and 1.40; group 5, between 1.40 and 1.75; and group 6, >1.75. Infant mortality rates for each group were 93.3%, 41.6%, 23.4%, 18.5%, 17.7%, and 14.2%, respectively (P < .0001). Maternal vitamin A deficiency during HIV infection may contribute to increased infant mortality.
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PMID:Infant mortality and maternal vitamin A deficiency during human immunodeficiency virus infection. 864 48

The presence of human immunodeficiency virus type 1 (HIV-1) in genital secretions may be a determinant of vertical HIV-1 transmission. Cervical and vaginal secretions from HIV-1-seropositive pregnant women were evaluated to determine prevalence and correlates of HIV-1-infected cells in the genital tract. HIV-1 DNA was detected by polymerase chain reaction in 32% of 212 cervical and 10% of 215 vaginal specimens. Presence of HIV-1 DNA in the cervix was associated with cervical mucopus and a significantly lower absolute CD4 cell count (354 vs. 469, P < .001). An absolute CD4 cell count <200 was associated with a 9.6-fold increased odds of cervical HIV-1 DNA detection compared with a count > or = 500 (95% confidence interval, 2.8-34.2). Detection of vaginal HIV- 1 DNA was associated with abnormal vaginal discharge, lower absolute CD4 cell count, and severe vitamin A deficiency. Presence of HIV-1-infected cells in genital secretions was associated with immunosuppression and abnormal cervical or vaginal discharge.
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PMID:Genital shedding of human immunodeficiency virus type 1 DNA during pregnancy: association with immunosuppression, abnormal cervical or vaginal discharge, and severe vitamin A deficiency. 898 96

Although low plasma vitamin A levels are associated with increased mortality and higher vertical transmission during human immunodeficiency virus (HIV) infection, it is unknown whether plasma low vitamin A levels are a marker for circulating HIV load. We conducted a cross-sectional study within a prospective cohort study of injection drug users in order to evaluate the relationship between plasma vitamin A levels and HIV viral load. Plasma vitamin A level was measured by high-performance liquid chromatography. Infectious viral load was measured by quantitative microculture of serial fivefold dilutions of 10(6) peripheral blood mononuclear cells. A total of 284 HIV-infected adults (79 women, 205 men) were studied. Plasma vitamin A levels consistent with deficiency were found in 28.9% of adults. A total of 38.0% of women and 25.3% of men had vitamin A deficiency (P < 0.04). The median infectious viral load for the entire study population was 8 infectious units per million cells. No significant relationship between plasma vitamin A levels and infectious viral load was observed in these injection drug users. This study suggests that there is no correlation between HIV viral load and plasma vitamin A levels in injection drug users, and these variables may represent independent risk factors during HIV infection. HIV-infected adult women appear to be at higher risk of developing vitamin A deficiency.
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PMID:Vitamin A levels and human immunodeficiency virus load in injection drug users. 900 89

Research related to maternal-child transmission of human immunodeficiency virus (HIV) has been advanced by standardization of case definitions and transmission rate calculation methodologies as well as enhanced diagnostic options for detecting infant HIV-1 infection. Standardization guidelines have yielded vertical transmission rate estimates of 25-30% in developing countries and 14-25% in developed countries. Mathematical modeling suggests that 95% of infant infections occur later than the last 2 months before delivery. Serial polymerase chain reaction evaluation has identified a 7.7% risk of in utero transmission, a 17.6% risk of combined in utero and intrapartum transmission, and a 4.9% incidence of late postnatal transmission. The risk of transmission through breast feeding has been estimated at 14%, with increases with longer durations. Advanced maternal clinical HIV status, primary infection, decreased maternal cell-mediated immunity, placentitis, ascending genital infection during the peripartum period, and syncytium-inducing HIV-1 strains have been associated with higher rates of maternal-child transmission. Prematurity, lack of cellular immunity, and vitamin A deficiency may be infant risk factors. The finding in an AIDS Clinical Trial Group that zidovudine (AZT) treatment was associated with a 67.5% reduction in risk has prompted widespread use of this regimen in developed countries; however, AZT is expensive and logistically difficult to administer in most developing country contexts. Randomized clinical trials currently underway are assessing the benefits of cesarean section delivery, postpartum HIV-specific immunoglobulin administration to infants, avoidance of breast feeding or early weaning, and antenatal maternal vitamin A administration. Selected intervention strategies should be regionally designed to take into account variations in viral, host, and obstetric factors.
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PMID:Mother-to-child transmission of human immunodeficiency virus type 1. 902 9

The complex puzzle of maternal factors involved in mother-to-child human immunodeficiency virus type 1 (HIV-1) transmission is being put together. The risk of perinatal infection increases with mother's disease progression, but it remains stable in women seroconverting to HIV-1 during pregnancy and in consecutive pregnancies. Thus, transmission correlates with the HIV-1 progression rather than the duration of infection in the mother. Nutritional alterations such as vitamin A deficiency may also have a significant impact, whereas geographic origin and mode of maternal infection are of no influence. Placenta membrane inflammation and concurrent sexually transmitted diseases are other significant covariates. The rate of transmission appears directly correlated with maternal age and inversely with length of gestation. A protective effect of caesarean section has been reported in some observational studies but, being controversial, these results need to be corroborated by randomized trials.
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PMID:Maternal clinical factors influencing HIV-1 transmission. 924 Aug 58


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