Maternal vitamin A deficiency and mother-to-child transmission of HIV-1

Semba, Richard D.; Chiphangwi, John D.; Miotti, Paolo; Dallabetta, Gina; Hoover, Donald R.; Canner, Joseph K.; Saah, A. J.

doi:10.1016/s0140-6736(94)93056-2

Cited by 378 publications

(98 citation statements)

References 24 publications

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“…Ligation-mediated PCR (LM-PCR)-Purified nuclei were resuspended at 10 8 nuclei/ml in 10 mM Tris (pH 7.4) 10 mM NaCl, 3 mM MgCl 2 , 10 mM CaCl 2 and 0.3 M sucrose and digested with the indicated concentrations of micrococcal nuclease for 20 min at 37°C. DNA was purified and treated with T4 polynucleotide kinase to phosphorylate the 5Ј-ends (36).…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Retinoic Acid Inhibition of Chromatin Remodeling at the Human Immunodeficiency Virus Type 1 Promoter

Kiefer

Hanley

Marcello

et al. 2004

Journal of Biological Chemistry

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All-trans retinoic acid (RA) represses HIV-1 transcription and replication in cultured monocytic cells and in primary monocyte-derived macrophages. Here we examine the role of histone acetylation and chromatin remodeling in RA-mediated repression. RA pretreatment of latently infected U1 promonocytes inhibits HIV-1 expression in response to the histone deacetylase (HDAC) inhibitor, trichostatin A (TSA). TSA is thought to activate HIV-1 transcription by inducing histone hyperacetylation within a regulatory nucleosome, nuc-1, positioned immediately downstream from the transcription start site. Acetylation of nuc-1 is thought to be a critical step in activation that precedes nuc-1 remodeling and, subsequently, transcriptional initiation. Here we demonstrate that TSA treatment induces H3 and H4 hyperacetylation and nuc-1 remodeling. Although RA pretreatment inhibits nuc-1 remodeling and HIV-1 transcription, it has no effect on histone acetylation. This suggests that acetylation and remodeling are not obligatorily coupled. We also show that growth of U1 cells in retinoid-deficient medium induces nuc-1 remodeling and HIV-1 expression but does not induce histone hyperacetylation. These findings suggest that remodeling, not histone hyperacetylation, is the limiting step in transcriptional activation in these cells. Together, these data suggest that RA signaling maintains the chromatin structure of the HIV-1 promoter in a transcriptionally non-permissive state that may contribute to the establishment of latency in monocyte/macrophages.

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Section: Methodsmentioning

confidence: 99%

“…Serum vitamin A levels have been inversely correlated with several properties of HIV-1-induced disease, including the degree of morbidity and mortality (7)(8)(9)(10)(11)(12)(13)(14)(15)(16). Moreover, vitamin A supplementation can reduce HIV-1 associated morbidity and mortality in children (12-14, 16 -19).…”

mentioning

confidence: 99%

Retinoic Acid Inhibition of Chromatin Remodeling at the Human Immunodeficiency Virus Type 1 Promoter

Kiefer

Hanley

Marcello

et al. 2004

Journal of Biological Chemistry

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“…Behavioural factors associated with vertical transmission include illicit drug use during pregnancy [16] and the presence of drug withdrawal symptoms in the infant [106]. Maternal age, over 30 years [61] and low vitamin A levels [102] have been positively correlated with transmission. The presence of maternal CMV and EBV coinfections were similarly correlated.…”

Section: Maternal Well-beingmentioning

confidence: 99%

HIV-1 Infection In Children: A Clinical and Immunologic Overview

Chakraborty¹

2005

Current HIV Research

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Globally, HIV-1 is most often transmitted heterosexually so that nearly half of all infected adults are women of child-bearing age. Infants may acquire infection from vertical transmission. Without treatment most HIV-1 infected children in Africa die before their third birthday; as a result child mortality has increased overall by 35-50%, and by greater than 100% in areas of high seroprevalence. HIV-1 infection has a heterogeneous spectrum of clinical course. Compared to HIV-1-infected adults, survival times are considerably shorter for children who acquire the virus perinatally or during infancy. Factors contributing to accelerated disease progression in infants and children are poorly understood but may include relative immunological immaturity, thymic HIV-1-mediated destruction at a time of active thymopoiesis, and HLA class I sharing between mother and infant. This review will initially discuss clinical and biological determinants of mother-to-child transmission and disease progression in HIV-infected infants and children. Our current knowledge of the mechanisms of T cell depletion is summarised and the host immune response to HIV-1 (innate and adaptive) described in the context of Pediatric HIV-1 infection.

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“…The therapeutic properties of Spirulina of some prospective studies were to treat certain pathological conditions including iron deficiency anemia [8,9], pernicious anemia [10], vitamin A deficiency [11][12][13], inhibition of mother-child transmission of HIV [14], inhibition of infection of T4 helper cells by HIV [15], protein energy disorders [16], cancer prevention through provision of carotenoids [17][18][19], radiological protection [20], and strengthening immune defenses [21][22][23].…”

Section: Introductionmentioning

confidence: 99%

Long-term effect of Spirulina platensis extract on DMBA-induced hamster buccal pouch carcinogenesis (immunohistochemical study)

et al. 2009

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In cancer research, the use of complementary and alternative medicine has increased over the past decade. In this study, 80 male golden Syrian hamsters were divided into four equal groups; the right buccal pouches of the hamster rats in group 1 were painted with 0.5% solution of 7, 12-dimethylbenz[a]anthracene (DMBA), three times a week for 32 weeks. The same pouches of group 2 were subjected to the same DMBA painting; but at the same time, the animals received 10 mg/daily Spirulina platensis extract for the same period. In group 3, the same regimen of DMBA painting was done but for 24 weeks only and the daily systemically S. platensis was received for the 32 weeks. In group 4, neither DMBA painting nor S. platensis administration was done but pouches were painted with saline and served as a control one. Five rats from each group were sacrificed at 12, 24, 28, and 32 weeks, respectively. The required pouches were excised, fixed, and embedded in paraffin to be immunostained with proliferating cell nuclear antigen (PCNA). The results showed that increased PCNA expression was directly related to the severity of pathological alterations from normal epithelium to dysplasia and from dysplasia to squamous cell carcinoma (SCC) in the study groups at the different extended periods of DMBA application and S. platensis extract administration. Analysis of variance and Duncan's multiple-range test for PCNA labeling index were proved a high significant difference (P < 0.01) between the different groups. From the previous results, it can be concluded that S. platensis extract has a beneficial role in regression of cancer progression.

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Maternal vitamin A deficiency and mother-to-child transmission of HIV-1

Cited by 378 publications

References 24 publications

Retinoic Acid Inhibition of Chromatin Remodeling at the Human Immunodeficiency Virus Type 1 Promoter

Retinoic Acid Inhibition of Chromatin Remodeling at the Human Immunodeficiency Virus Type 1 Promoter

HIV-1 Infection In Children: A Clinical and Immunologic Overview

Long-term effect of Spirulina platensis extract on DMBA-induced hamster buccal pouch carcinogenesis (immunohistochemical study)

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