Kannagi M, Kiyotaki M, King N W, Lord C I, Letvin N L
J Virol. 1987 May;61(5):1421-6. doi: 10.1128/JVI.61.5.1421-1426.1987.
The human immunodeficiency virus (HIV) and the closely related simian immunodeficiency virus (SIV) induce profound immune dysfunction in primate species. The present studies show that cell populations infected in vitro with SIV exhibit increases in major histocompatibility complex (MHC) class II antigen expression. Cell lines chronically infected with both the monkey and human viruses express substantially more MHC class II but not more lineage-restricted or activation antigens on their membranes than do uninfected cell lines. Furthermore, 2'-deoxy-5-iodouridine increased MHC class II antigen expression on SIV-infected cell lines in parallel with increased expression of viral antigens. MHC class II induction does not appear to be mediated through the production of a soluble factor, such as gamma interferon, by SIV-infected cells. Interestingly, studies of the kinetics of antigen expression by cell lines after SIV infection indicate that the induction of MHC class II structures is a late event. Immunoelectron microscopy revealed that MHC class II antigen is expressed not only on the surfaces of the SIV-infected cells but also on the envelope of virus particles derived from those cells. MHC antigen expression on virus-infected cells and the expression of those determinants by the virus may play a role in the pathogenesis of acquired immunodeficiency syndrome and the autoimmune abnormalities observed in HIV-infected individuals.
人类免疫缺陷病毒（HIV）和密切相关的猿猴免疫缺陷病毒（SIV）可在灵长类动物中引发严重的免疫功能障碍。目前的研究表明，体外感染SIV的细胞群体主要组织相容性复合体（MHC）II类抗原表达增加。长期感染猴病毒和人病毒的细胞系在其细胞膜上表达的MHC II类抗原显著增多，但谱系限制性抗原或活化抗原并不比未感染的细胞系更多。此外，2'-脱氧-5-碘尿苷可使SIV感染的细胞系上的MHC II类抗原表达增加，同时病毒抗原的表达也增加。MHC II类抗原的诱导似乎不是由SIV感染的细胞产生可溶性因子（如γ干扰素）介导的。有趣的是，对SIV感染后细胞系抗原表达动力学的研究表明，MHC II类结构的诱导是一个晚期事件。免疫电子显微镜显示，MHC II类抗原不仅在SIV感染细胞的表面表达，也在源自这些细胞的病毒颗粒包膜上表达。病毒感染细胞上的MHC抗原表达以及病毒对这些决定簇的表达可能在获得性免疫缺陷综合征的发病机制以及HIV感染个体中观察到的自身免疫异常中发挥作用。
