Brooks David G, Zack Jerome A
Department of Microbiology, Immunology and Molecular Genetics, School of Medicine, University of California at Los Angeles, Los Angeles, California 90095, USA.
J Virol. 2002 Feb;76(4):1673-81. doi: 10.1128/jvi.76.4.1673-1681.2002.
Highly active antiretroviral therapy has succeeded in many cases in suppressing virus production in patients infected with human immunodeficiency virus (HIV); however, once treatment is discontinued, virus replication is rekindled. One reservoir capable of harboring HIV in a latent state and igniting renewed infection once therapy is terminated is a resting T cell. Due to the sparsity of T cells latently infected with HIV in vivo, it has been difficult to study viral and cellular interactions during latency. The SCID-hu (Thy/Liv) mouse model of HIV latency, however, provides high percentages of latently infected cells, allowing a detailed analysis of phenotype. Herein we show that latently infected cells appear phenotypically normal. Following cellular stimulation, the virus completes its life cycle and induces phenotypic changes, such as CD4 and major histocompatibility complex class I down-regulation, in the infected cell. In addition, HIV expression following activation did not correlate with expression of the cellular activation marker CD25. The apparently normal phenotype and lack of HIV expression in latently infected cells could prevent recognition by the immune response and contribute to the long-lived nature of this reservoir.
高效抗逆转录病毒疗法在许多情况下成功抑制了感染人类免疫缺陷病毒（HIV）患者体内的病毒产生；然而，一旦停止治疗，病毒复制就会重新燃起。静息T细胞是一种能够在潜伏状态下隐匿HIV并在治疗终止后引发新一轮感染的储存库。由于体内潜伏感染HIV的T细胞稀少，很难研究潜伏期的病毒与细胞相互作用。然而，HIV潜伏期的SCID-hu（Thy/Liv）小鼠模型提供了高比例的潜伏感染细胞，从而能够对表型进行详细分析。在此我们表明，潜伏感染的细胞在表型上看似正常。细胞受到刺激后，病毒完成其生命周期并在感染细胞中诱导表型变化，如CD4和I类主要组织相容性复合体下调。此外，激活后HIV的表达与细胞激活标志物CD25的表达无关。潜伏感染细胞中明显正常的表型以及缺乏HIV表达可能会阻止免疫反应的识别，并导致这个储存库具有长期存在的特性。
