Chen Lien-Cheng, Shyu Huey-Wen, Chen Shun-Hua, Lei Huan-Yao, Yu Chun-Keung, Yeh Trai-Ming
Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
J Med Virol. 2006 Jun;78(6):780-6. doi: 10.1002/jmv.20623.
T-cell depletion is found in enterovirus 71 (EV71)-infected patients with pulmonary edema. However, the mechanism that causes T-cell depletion is unclear. To address this question, the effects of EV71 infection on the cell viability of human Jurkat T cells were studied. Viable viruses were recovered from both the culture supernatant and the cell lysate of Jurkat cells after EV71 infection. Results from reverse-transcription polymerase chain reaction (RT-PCR) and immunofluorescence assay confirmed further the presence of EV71 negative-strand RNA and antigen, respectively, in EV71-infected Jurkat cells. The viability of the Jurkat cells decreased after 48 hr of EV71 infection. Both terminal transferase end labeling (TUNEL) and DNA fragmentation assays demonstrated that the apoptosis of EV71-infected Jurkat cells had increased. In addition, the expression of Fas ligand (FasL) in EV71-infected Jurkat cells increased at both mRNA and surface expression levels. Taken together, these results confirmed that EV71 infected T cells and induced FasL expression, which may contribute to T-cell apoptosis during EV71 infection.
在感染肠道病毒71型（EV71）并出现肺水肿的患者中发现T细胞耗竭。然而，导致T细胞耗竭的机制尚不清楚。为了解决这个问题，研究了EV71感染对人Jurkat T细胞活力的影响。EV71感染后，从Jurkat细胞的培养上清液和细胞裂解物中均回收了活病毒。逆转录聚合酶链反应（RT-PCR）和免疫荧光分析结果分别进一步证实了EV71感染的Jurkat细胞中存在EV71负链RNA和抗原。EV71感染48小时后，Jurkat细胞的活力下降。末端脱氧核苷酸转移酶介导的缺口末端标记法（TUNEL）和DNA片段化分析均表明，EV71感染的Jurkat细胞凋亡增加。此外，EV71感染的Jurkat细胞中Fas配体（FasL）的mRNA表达水平和表面表达水平均升高。综上所述，这些结果证实EV71感染T细胞并诱导FasL表达，这可能是EV71感染期间T细胞凋亡的原因。
