Enterovirus 71 infection induces Fas ligand expression and apoptosis of Jurkat cells

Journal of Medical Virology
Lien-Cheng ChenTrai-Ming Yeh

Abstract

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.

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Citations

Aug 6, 2010·Clinical and Vaccine Immunology : CVI·Shih-Min WangChing-Chuan Liu
Nov 1, 2011·World Journal of Gastroenterology : WJG·Jing LuMing-Liang He
Mar 24, 2012·Future Microbiology·Hsing-I HuangShin-Ru Shih
Jun 10, 2011·Critical Reviews in Microbiology·Lina YiMing-Liang He
Jun 22, 2007·Cellular Microbiology·Tsan-Chi ChenJyh-Lyh Juang
Jun 23, 2009·Nature Medicine·Yorihiro NishimuraHiroyuki Shimizu
Aug 18, 2009·Expert Review of Anti-infective Therapy·Shih-Min Wang, Ching-Chuan Liu
Oct 19, 2017·Experimental and Therapeutic Medicine·Zengjun JinWeihao Li
Apr 19, 2020·Molecular Therapy : the Journal of the American Society of Gene Therapy·Xiaowei ZhangZongqiang Cui

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Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis