Piguet V, Trono D
Department of Dermatology, DHURDV, University of Geneva, Geneva, Switzerland.
Semin Immunol. 2001 Feb;13(1):51-7. doi: 10.1006/smim.2000.0295.
The human and simian immunodeficiency viruses (HIV and SIV, respectively) are members of the lentiviridae subgroup of retroviruses that cause a progressive failure of the host immunological functions culminating in the clinical collapse known as AIDS, or acquired immunodeficiency syndrome. In the absence of antiviral therapy, this course is inexorable in spite of an initially vigorous immune response. Two fundamental characteristics of the biology of primate lentiviruses explain this apparent paradox. First, HIV and SIV infect CD4(+)targets such as helper T lymphocytes and macrophages, that is, cells that normally play an essential role in the emergence and maintenance of an effective antiviral response. Second, these viruses have evolved a number of strategies to evade control by the immune system. These include mutational escape, latency, masking of antibody-binding sites on the viral envelope, downmodulation of the class I major histocompatibility complex (MHC-I), and upregulation of the Fas ligand on the surface of infected cells. Examining the mechanisms of these phenomena not only helps to understand how HIV wins its war against the immune system, but it also suggests as yet unexploited avenues to combat the virus through therapies and to develop a vaccine.
人类免疫缺陷病毒和猿猴免疫缺陷病毒(分别为HIV和SIV)是逆转录病毒慢病毒亚组的成员,它们会导致宿主免疫功能逐渐衰退,最终引发被称为艾滋病(即获得性免疫缺陷综合征)的临床崩溃。在没有抗病毒治疗的情况下,尽管最初免疫反应强烈,但病程仍不可避免。灵长类慢病毒生物学的两个基本特征解释了这一明显的矛盾。首先,HIV和SIV感染CD4(+)靶细胞,如辅助性T淋巴细胞和巨噬细胞,即通常在有效抗病毒反应的产生和维持中起关键作用的细胞。其次,这些病毒已经进化出多种逃避免疫系统控制的策略。这些策略包括突变逃逸、潜伏、掩盖病毒包膜上的抗体结合位点、下调I类主要组织相容性复合体(MHC-I)以及上调受感染细胞表面的Fas配体。研究这些现象的机制不仅有助于理解HIV如何在与免疫系统的对抗中获胜,还能为通过治疗对抗该病毒以及开发疫苗提供尚未开发的途径。