Kopnisky Kathy L, Stoff David M, Rausch Dianne M
Center for Mental Health Research on AIDS, National Institute of Mental Health, 6001 Executive Blvd, MSC 9619, Bethesda, MD 20892-9619, USA.
Brain Behav Immun. 2004 May;18(3):246-61. doi: 10.1016/j.bbi.2003.08.003.
The reciprocal interactions between the neuroendocrine, immune, and autonomic nervous systems are complicated, yet worthy of examination. A body of literature suggests that psychological factors such as stress, or psychiatric conditions such as major depression, may influence the immune system thereby altering host susceptibility to viral, or other types of infection. Alternately, in an attempt to limit infection and replication, the anti-viral host response, via innate and acquired immunity and subsequent release of pro-inflammatory cytokines and additional anti-viral mediators, may affect mood, cognition emotion, and possibly precipitate a psychiatric disorder. In order to address what is known regarding neuroendocrine-immune interactions in the context of HIV infection, the Center for Mental Health Research on AIDS convened a panel of scientists from diverse areas of expertise. Their primary charge was to examine whether stress-induced activation of the neuroendocrine system affects the immune system in a manner that negatively influences HIV disease progression, and whether HIV infection influences the central nervous system and behavior. The ensuing report summarizes their deliberations as they discussed the current body of information and identified outstanding critical questions in the areas of research. The group consensus was that the biological mediators of psychological status can play an important role in mediating HIV disease progression, particularly in subgroups of vulnerable patients; furthermore, they identified candidate biological mediators and mechanisms of disease progression. The Workgroup outlined the inherent challenges and limitations of such research and provided recommendations as to the future directions of research utilizing human, animal, and in vitro models of HIV-1 infection and stress.
神经内分泌系统、免疫系统和自主神经系统之间的相互作用错综复杂,但值得研究。大量文献表明,压力等心理因素或重度抑郁症等精神疾病可能会影响免疫系统,从而改变宿主对病毒或其他类型感染的易感性。反过来,为了限制感染和复制,抗病毒宿主反应通过先天免疫和后天免疫以及随后促炎细胞因子和其他抗病毒介质的释放,可能会影响情绪、认知和情感,并可能引发精神障碍。为了探讨在艾滋病毒感染背景下已知的神经内分泌 - 免疫相互作用,艾滋病心理健康研究中心召集了一批来自不同专业领域的科学家。他们的主要任务是研究压力诱导的神经内分泌系统激活是否以对艾滋病毒疾病进展产生负面影响的方式影响免疫系统,以及艾滋病毒感染是否影响中枢神经系统和行为。随后的报告总结了他们的讨论,他们讨论了当前的信息,并确定了该研究领域中尚未解决的关键问题。小组达成的共识是,心理状态的生物介质在介导艾滋病毒疾病进展中可以发挥重要作用,特别是在脆弱患者亚组中;此外,他们确定了疾病进展的候选生物介质和机制。该工作组概述了此类研究固有的挑战和局限性,并就利用艾滋病毒 -1感染和压力的人类、动物和体外模型进行研究的未来方向提出了建议。