Darko D F, Mitler M M, Henriksen S J
Scripps Research Institute, La Jolla, CA 92037-1027, USA.
Adv Neuroimmunol. 1995;5(1):57-77. doi: 10.1016/0960-5428(94)00044-o.
The aberrant sleep documented in subjects with human immunodeficiency virus (HIV) infection is uniquely important because of the contribution this poor quality sleep makes to the fatigue, disability, and eventual unemployment that befalls these patients. Especially given this importance in clinical care, the research on the prominent sleep changes described in HIV infection remains modest in quantity. The chronic asymptomatic stage of HIV infection is associated with the most intriguing and singular sleep structure changes. Especially robust is the increase in slow wave sleep, particularly in latter portions of the sleep period. This finding is rare in other primary or secondary sleep disorders. The sleep structure alterations are among the most replicable of several pathophysiological sequelae in the brain associated with early HIV infection. It is unlikely that these sleep architecture changes are psychosocial in etiology, and they occur before medical pathology is evident. They are not associated with stress, anxiety, or depression. Evidence is accumulating to support a role for the somnogenic immune peptides tumor necrosis factor (TNF)alpha and interleukin (IL-1 beta) in the sleep changes and fatigue commonly seen in HIV infection. These peptides are elevated in the blood of HIV-infected individuals, and are somnogenic in clinical use and animal models. The peripheral production of these peptides may also have a role in the regulation of normal sleep physiology. The lentivirus family contains both HIV and the feline immunodeficiency virus (FIV). The use of the FIV model of HIV infection may provide a way to further investigate the mechanism of a neurotropic, neurotoxic virus initiating the immune acute phase response and affecting sleep. Neurotropic lentivirus infection is a microbiological probe facilitating neuroimmune investigation.
人类免疫缺陷病毒（HIV）感染者出现的异常睡眠尤为重要，因为这种睡眠质量差会导致这些患者出现疲劳、残疾并最终失业。鉴于其在临床护理中的重要性，关于HIV感染中显著睡眠变化的研究数量仍然有限。HIV感染的慢性无症状阶段与最引人关注且独特的睡眠结构变化有关。尤其明显的是慢波睡眠增加，特别是在睡眠后期。这一发现在其他原发性或继发性睡眠障碍中很少见。睡眠结构改变是与早期HIV感染相关的大脑几种病理生理后遗症中最具重复性的现象之一。这些睡眠结构变化在病因上不太可能是社会心理因素导致的，且在医学病理表现明显之前就已出现。它们与压力、焦虑或抑郁无关。越来越多的证据支持促睡眠免疫肽肿瘤坏死因子（TNF）α和白细胞介素（IL-1β）在HIV感染中常见的睡眠变化和疲劳中起作用。这些肽在HIV感染者的血液中升高，在临床应用和动物模型中具有促睡眠作用。这些肽的外周产生可能也在正常睡眠生理调节中发挥作用。慢病毒家族包括HIV和猫免疫缺陷病毒（FIV）。使用HIV感染的FIV模型可能为进一步研究嗜神经、神经毒性病毒引发免疫急性期反应并影响睡眠的机制提供一种方法。嗜神经慢病毒感染是一种有助于神经免疫研究的微生物学探针。
