Vitamin A Deficiency in Non-Vitamin-Supplemented Patients with AIDS

Karter, Dennis; Karter, Andrew J.; Yarrish, Robert; Patterson, Clair C.; Kass, Philip H.; Nord, Jill A.; Kislak, Jay Ward

doi:10.1097/00042560-199502000-00012

Cited by 29 publications

(16 citation statements)

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“…In previous publications (4,5,(17)(18)(19)(20)(21), the terms hyporetinemia and hyporetinolemia have been used interchangeably to describe the reduction in circulating retinol during inflammation. Etymologically, the term hyporetinolemia is specific in referring to retinol, whereas hyporetinemia implies a reduction in VA including retinol, retinyl esters, and retinoic acid.…”

Section: Discussionmentioning

confidence: 99%

“…The pathogenesis of various infections, such as measles and malaria, is also accompanied by hyporetinolemia. Clinical consequences of this hyporetinolemia are an increase in morbidity (i.e., duration of hospitalization) and mortality of children in poor and rich nations (4,5). In the case of measles infections, supplementation with VA reduces both morbidity and mortality (4).…”

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confidence: 99%

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Accumulation of retinol in the liver after prolonged hyporetinolemia in the vitamin A-sufficient rat

Gieng

Raila

Rosales

2005

Journal of Lipid Research

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We assessed the effects of prolonged reduction of plasma retinol concentrations (hyporetinolemia) on the distribution of tissue vitamin A (VA) and of its active compounds using a model of continuous recombinant human interleukin-6 (rhIL-6) infusion via osmotic minipumps in VAsufficient male rats. Plasma retinol and retinol-binding protein (RBP) concentrations remained decreased and lower in rhIL-6-treated rats compared with controls from 7.5 h throughout 7 days of infusion ( P Ͻ 0.001). This reduction was accompanied by a 68% increase in hepatic retinol concentration by 7 days ( P Ͻ 0.05). Hepatic and renal retinyl palmitate and retinoic acid concentrations did not change, and renal megalin content remained unchanged; hepatic RBP concentrations were 41% lower in rhIL-6-treated rats compared with controls ( P Ͻ 0.05). These results indicate that instead of being lost, retinol accumulated in the liver during inflammation and that hyporetinolemia was attributable to a decrease in the availability of hepatic RBP. A plausible consequence of the effect of rhIL-6-induced hyporetinolemia is that by 7 days tissues that are dependent on plasma retinol may become deprived of VA. These results have important implications in understanding the mechanism by which measles infection induces hyporetinolemia and VA deficiency of extrahepatic tissues. -Gieng, S. H., J. Raila, and F. J. Rosales. Accumulation of retinol in the liver after prolonged hyporetinolemia in the vitamin A-sufficient rat. J. Lipid Res. 2005. 46: 641-649.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Accumulation of retinol in the liver after prolonged hyporetinolemia in the vitamin A-sufficient rat

Gieng

Raila

Rosales

2005

Journal of Lipid Research

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“…The potential effect of vitamin A on lymphocyte counts in adults has been studied among HIV-infected individuals, who are at high risk of developing profound nutritional deficiencies (51,71,135). Single-dose supplementation with vitamin A in nonpregnant HIV-positive women (65) and injection drug users (129) did not have a significant effect on CD4 cell counts; however, daily supplementation with vitamin A during 6 weeks in Kenyan HIV-infected women resulted in a modest, marginally significant greater mean CD4 cell count (5).…”

Section: T and B Lymphocytesmentioning

confidence: 99%

Effects of Vitamin A Supplementation on Immune Responses and Correlation with Clinical Outcomes

2005

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Vitamin A supplementation to preschool children is known to decrease the risks of mortality and morbidity from some forms of diarrhea, measles, human immunodeficiency virus (HIV) infection, and malaria. These effects are likely to be the result of the actions of vitamin A on immunity. Some of the immunomodulatory mechanisms of vitamin A have been described in clinical trials and can be correlated with clinical outcomes of supplementation. The effects on morbidity from measles are related to enhanced antibody production and lymphocyte proliferation. Benefits for severe diarrhea could be attributable to the functions of vitamin A in sustaining the integrity of mucosal epithelia in the gut, whereas positive effects among HIV-infected children could also be related to increased T-cell lymphopoiesis. There is no conclusive evidence for a direct effect of vitamin A supplementation on cytokine production or lymphocyte activation. Under certain circumstances, vitamin A supplementation to infants has the potential to improve the antibody response to some vaccines, including tetanus and diphtheria toxoids and measles. There is limited research on the effects of vitamin A supplementation to adults and the elderly on their immune function; currently available data provide no consistent evidence for beneficial effects. Additional studies with these age groups are needed

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“…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).…”

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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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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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Vitamin A Deficiency in Non-Vitamin-Supplemented Patients with AIDS

Cited by 29 publications

References 0 publications

Accumulation of retinol in the liver after prolonged hyporetinolemia in the vitamin A-sufficient rat

Accumulation of retinol in the liver after prolonged hyporetinolemia in the vitamin A-sufficient rat

Effects of Vitamin A Supplementation on Immune Responses and Correlation with Clinical Outcomes

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

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