Via C S, Morse H C, Shearer G M
Division of Rheumatology and Clinical Immunology, University of Maryland School of Medicine and Research Service, Loch Raven VA Medical Center, Baltimore 21201.
Immunol Today. 1990 Jul;11(7):250-5. doi: 10.1016/0167-5699(90)90099-u.
After initial infection with human immunodeficiency virus 1 (HIV-1), patients may remain asymptomatic for years before the onset of acquired immune deficiency syndrome (AIDS). This non-aggressive or latent phase may be manifested by functional abnormalities of both T and B cells, even in the absence of critical reductions in lymphocyte numbers. At present, it is not clear whether the immune abnormalities in either the asymptomatic phase or in clinical AIDS are due solely to direct effects of HIV-1 or whether they also reflect host immunoregulatory mechanisms. In this article, by Charles Via, Herbert Morse and Gene Shearer, the immune abnormalities associated with early HIV-1 infection are compared with immune abnormalities found in three murine models of autoimmunity and immunodeficiency, and it is suggested that host mechanisms contribute to defective helper T (TH)-cell function early in the course of HIV-1 infection. Furthermore, two murine models appear relevant to the study of late HIV-1 infection and suggest a role for CD8+ T cells in the prevention of symptomatic AIDS.
在初次感染人类免疫缺陷病毒1型（HIV-1）后，患者在获得性免疫缺陷综合征（AIDS）发作前可能多年无症状。即使淋巴细胞数量没有显著减少，这个非侵袭性或潜伏期也可能表现为T细胞和B细胞的功能异常。目前尚不清楚无症状期或临床AIDS期的免疫异常是仅由HIV-1的直接作用引起，还是也反映了宿主免疫调节机制。在Charles Via、Herbert Morse和Gene Shearer撰写的这篇文章中，将早期HIV-1感染相关的免疫异常与三种自身免疫和免疫缺陷小鼠模型中发现的免疫异常进行了比较，并提出宿主机制在HIV-1感染过程早期导致辅助性T（TH）细胞功能缺陷。此外，两种小鼠模型似乎与晚期HIV-1感染的研究相关，并提示CD8+ T细胞在预防症状性AIDS中发挥作用。
