Fauci A S
Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.
Lymphokine Res. 1990 Winter;9(4):527-31.
Infection with the human immunodeficiency virus (HIV) is characterized by a long and variable asymptomatic phase followed by the development of the acquired immunodeficiency syndrome (AIDS) in a substantial proportion of individuals within 10 years. An understanding of the mechanism by which the infection progresses in vivo to an ultimate destruction of the immune system is essential to the design of rational approaches to anti-viral therapy, immune reconstitution, and vaccine development. To delineate these complex processes, we have established an in vitro model of latent or chronic HIV infection and have used this model to examine ways in which HIV replication can be upregulated. We have shown that cytokines are important mediators of HIV replication in chronically HIV-infected cells. Thus, the virus has incorporated itself into the human immune system and utilizes for its own propagation many of the cellular and molecular mechanisms which the immune system uses to maintain its homeostatic regulation. Studies in this area will not only shed important light on the immunopathogenesis of HIV, but will certainly lead to greater depth in our understanding of the normal function of the human immune system.
人类免疫缺陷病毒（HIV）感染的特征是存在一个漫长且多变的无症状期，随后相当一部分个体在10年内会发展为获得性免疫缺陷综合征（AIDS）。了解该感染在体内如何进展至最终破坏免疫系统的机制，对于设计合理的抗病毒治疗、免疫重建及疫苗研发方法至关重要。为了阐明这些复杂过程，我们建立了一个潜伏或慢性HIV感染的体外模型，并利用该模型研究上调HIV复制的方法。我们已经表明，细胞因子是慢性HIV感染细胞中HIV复制的重要介质。因此，该病毒已融入人类免疫系统，并利用免疫系统用于维持其稳态调节的许多细胞和分子机制来实现自身繁殖。该领域的研究不仅将为HIV的免疫发病机制提供重要线索，而且必将使我们对人类免疫系统正常功能的理解更加深入。
