DeCotiis Jennifer L, Ortiz Noelle C, Vega Brian A, Lukac David M
Dept. of Microbiology, Biochemistry, and Molecular Genetics, Graduate School of Biomedical Sciences, Rutgers Biomedical and Health Sciences, Rutgers University, New Jersey Medical School, 225 Warren St., ICPH E 350C, Newark, NJ, 07103, USA.
Dept. of Microbiology, Biochemistry, and Molecular Genetics, Graduate School of Biomedical Sciences, Rutgers Biomedical and Health Sciences, Rutgers University, New Jersey Medical School, 225 Warren St., ICPH E 350C, Newark, NJ, 07103, USA.
J Virol Methods. 2017 Sep;247:99-106. doi: 10.1016/j.jviromet.2017.04.019. Epub 2017 Jun 8.
Reactivation of Kaposi's sarcoma-associated herpesvirus (KHSV; also known as Human herpesvirus (HHV)-8) from latency is associated with progression to disease. The primary experimental models for studying KSHV reactivation are B lymphocyte cell lines derived from patients with primary effusion lymphoma (PEL). PEL models have remained essential tools for understanding molecular details of latency and reactivation, yet they have shortcomings. In particular, PEL cells are difficult to transfect with plasmid DNA, which limits their routine use in studies that require introduction of exogenous DNA. Moreover, PELs produce poorly infectious virus, which limits functional quantitation of the ultimate step in KSHV reactivation. In this study, we show that a recently published reporter virus system overcomes inherent difficulties of using PELs for studying viral reactivation. Vero rKSHV.294 cells harbor a recombinant reporter KSHV clone and produce infectious virus whose quantitation is strictly dependent on passage to naïve 293 cells. We show that the cells are easily transfectable, and produce significant amount of infectious virus in response to ectopically-expressed lytic switch protein Rta. In thus study, we derive optimal conditions to measure fold reactivation by varying experimental time periods and media volumes in infections and reporter enzyme reactions, and by eliminating background cellular and media activities. By measuring production of infectious virus, we demonstrate that Rta, but not the cellular transactivator Notch Intracellular Domain (NICD)-1, is sufficient to reactivate KSHV from latency. These data confirm previous studies that were limited to measuring viral gene expression in PELs as indicators of reactivation.
卡波西肉瘤相关疱疹病毒(KSHV;也称为人类疱疹病毒(HHV)-8)从潜伏状态重新激活与疾病进展相关。研究KSHV重新激活的主要实验模型是源自原发性渗出性淋巴瘤(PEL)患者的B淋巴细胞系。PEL模型仍然是理解潜伏和重新激活分子细节的重要工具,但它们存在缺点。特别是,PEL细胞难以用质粒DNA转染,这限制了它们在需要引入外源DNA的研究中的常规使用。此外,PEL产生的病毒感染性较差,这限制了KSHV重新激活最终步骤的功能定量。在本研究中,我们表明最近发表的报告病毒系统克服了使用PEL研究病毒重新激活的固有困难。Vero rKSHV.294细胞携带重组报告KSHV克隆,并产生感染性病毒,其定量严格依赖于传代至未感染的293细胞。我们表明这些细胞易于转染,并在响应异位表达的裂解开关蛋白Rta时产生大量感染性病毒。在本研究中,我们通过改变感染和报告酶反应中的实验时间段和培养基体积,并消除背景细胞和培养基活性,得出了测量重新激活倍数的最佳条件。通过测量感染性病毒的产生,我们证明Rta而非细胞反式激活因子Notch细胞内结构域(NICD)-1足以使KSHV从潜伏状态重新激活。这些数据证实了先前仅限于测量PEL中病毒基因表达作为重新激活指标的研究。