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Enterovirus 71 infection induces Fas ligand expression and apoptosis of Jurkat cells
Author(s) -
Chen LienCheng,
Shyu HueyWen,
Chen ShunHua,
Lei HuanYao,
Yu ChunKeung,
Yeh TraiMing
Publication year - 2006
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.20623
Subject(s) - jurkat cells , virology , apoptosis , fas ligand , enterovirus , ligand (biochemistry) , biology , virus , programmed cell death , immunology , t cell , genetics , receptor , immune system
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. J. Med. Virol. 78:780–786, 2006. © 2006 Wiley‐Liss, Inc.