IMPACT OF MICRONUTRIENTS ON PROGRESSION OF SIV

描述：(摘自所提供的摘要) 对HIV感染患者的研究表明，血清 微量营养素水平往往低于正常水平，特别是在 维生素A、B12、E和硒。一些研究的相关性很低。 微量营养素水平与艾滋病毒感染进展更快有关。 用微量营养素进行干预试验极其困难。 由于以下原因，艾滋病毒携带者中的出生率很高： 的艾滋病毒/艾滋病患者已经在服用营养补充剂 不受控制的方式，有些是大剂量；年微量营养素的摄入量 HIV感染者的食物差异很大；有复杂的 围绕微量营养素安慰剂对照试验的伦理问题 在艾滋病毒/艾滋病人群中；很难保持一个 HIV发展过程中的微量营养素干预研究 感染；以及当前和迅速变化的抗逆转录病毒疗法 将改变艾滋病毒的自然历史，使分离出来变得复杂 微量营养素干预的效果。然而，微量营养素 补充剂可能在改善整体健康状况方面发挥重要作用 营养状况和减缓艾滋病毒感染的进程。这个 猴免疫缺陷病毒(SIV)在青少年中引起感染 猕猴与人类免疫缺陷病毒引起的 人类，包括我们最近发现的血清微量营养素 尽管摄入量明显充足，但仍存在缺陷。SIV还会导致 消瘦的情况类似于艾滋病毒携带者的年轻人。 由于SIV的快速发展和明确的终点 营养参数、生物标志物和存活率，以及 控制饮食摄入量，感染SIV的恒河猴是理想的 研究补充微量营养素的潜在益处的模型。 为此，我们计划：1)记录微量营养素的过程 SIV感染幼年恒河猴的缺陷和体重减轻 与年龄匹配的未感染的对照动物进行比较；以及2)进行3 对感染SIV的猕猴进行微量营养素干预，包括 维他命和微量矿物质的高度补充；单一的 肌肉补充维生素B12；以及单一的 补充硒。终点包括死亡时间；体重 瘦体质量；血清微量营养素；病毒载量；CD4细胞计数； 以及机会性感染的发展。 这些研究将有助于评估微量营养素的疗效。 不含混杂因子的猴SIV模型中的补充剂 参与了一项关于人类艾滋病毒感染的研究。此外，自然的 营养缺乏和消瘦的历史可以用这个来定义 该模型为营养学的进一步研究奠定了基础。 干预措施。

DESCRIPTION : (duplicated from the abstract provided) Studies in patients with HIV infection have revealed that serum micronutrient levels are often below normal levels particularly for vitamins A, B12, E and for selenium. Some studies have correlated low micronutrient levels with more rapid progression of HIV infection. Intervention trials with micronutrients are extremely difficult to carry out in persons with HIV for the following reasons : a large percentage of HIV/AIDS patients are already taking nutritional supplements in an uncontrolled manner, some in large doses; intake of micronutrients in food varies greatly among persons with HIV infection; there are complex ethical issues surrounding a placebo controlled trial of micronutrients in the HIV/AIDS population; it would be difficult to maintain a micronutrient intervention study during the years of progression of HIV infection; and current and rapidly changing anti-retroviral therapies will alter the natural history of HIV, making it complex to separate out the effects of micronutrient intervention. Yet, micronutrient supplements might play an important role in improving overall nutritional status and slowing the progression of HIV infection. The Simian immunodeficiency virus (SIV) produces an infection in juvenile rhesus monkeys that is remarkably similar to that caused by HIV in humans including, as we have found recently, serum micronutrient deficiencies despite an apparently adequate intake. SIV also causes a wasting condition similar to that seen in young persons with HIV. Because of the rapid progression in SIV, and the clear end points of nutritional parameters, biological markers, and survival, as well as a controlled dietary intake, the SIV-infected rhesus monkey is an ideal model to examine the potential benefit of micronutrient supplementation. To this end we plan to: 1) document the course of micronutrient deficiency and weight loss in SIV-infected juvenile rhesus macaques compared to age matched uninfected control animals; and 2) conduct 3 interventions with micronutrients in SIV infected macaques, including a high supplementation with vitamins and trace minerals; single supplementation with vitamin B12 intramuscularly; and a single supplementation selenium. End points include time of death; body weight and lean body mass; serum micronutrients; viral load; CD4 cell count; and development of opportunistic infections. These studies will allow the evaluation of the efficacy of micronutrient supplements in the monkey SIV model without the confounding factors involved in a study in human HIV infection. In addition, the natural history of nutritional deficits and wasting would be defined in this model, which would provide a basis for further studies on nutritional interventions.