期刊
PLOS ONE
卷 11, 期 3, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0152177
关键词
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资金
- National Natural Science Foundation of China [81571993]
- Mega Infectious Diseases Program from the Ministry of Science of Technology of China [2014ZX10004001-002]
- Natural Science Foundation of Jiangsu Province [BK20141078]
Enterovirus 71 (EV71) causes hand-foot-and-mouth disease, which can lead to fatal neurological complications in young children and infants. Few gastrointestinal symptoms are observed clinically, suggesting the presence of a unique immunity to EV71 in the gut. We reported a robust induction of interferons (IFNs) in human intestinal epithelial cells (HT-29), which was suppressed in other types such as RD and HeLa cells. The underlying mechanism for the apparent difference remains obscure. In this study we report that in EV71-infected HT-29 cells, TLR/TRIF signaling was essential to IFN induction; viral replication increased and the induction of IFN-alpha, -beta, -omega, -kappa, and -epsilon decreased markedly in TRIF-silenced HT-29 cells. Importantly, TRIF was degraded by viral 3C(pro) in RD cells, but resisted cleavage, and IRF3 was activated and translocated into the nucleus in HT-29 cells. Taken together, our data suggest that IFNs were induced differentially in human HT-29 cells through an intact TLR/TRIF signaling, which differs from other cell types and may be implicated in viral pathogenesis in EV71 infection.
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