Open AccessThe inhibiting effect of the transcription factor p53 on dengue virus infection by activating the type I interferon
Author(s) -
Yanling Hu,
Xiaoshan Li,
Shunbin Xiong,
Qiang Ma,
Dan Liŭ,
Zhong-Quan Shi,
Jing Tang,
Xiancai Rao,
Fuquan Hu,
Guoli Li
Publication year - 2017
Publication title -
oncotarget
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.373
H-Index - 127
ISSN - 1949-2553
DOI - 10.18632/oncotarget.15352
Subject(s) - interferon , virology , immunofluorescence , apoptosis , biology , dengue virus , western blot , rna interference , virus , viral interference , cell culture , vero cell , microbiology and biotechnology , cell , dengue fever , rna , viral replication , immunology , antibody , gene , biochemistry , genetics
To investigate the role of the transcription factor p53 in the course of the dengue virus (DV) infection. The human hepatocellular carcinoma cell strain HepG2 with a low expression level of p53 was built by using the retroviral-mediated RNA interference technology, and was detected by Western blot. The wild group and the interference group were respectively infected by the type 2 DV. The viral titration was detected by the Vero plaque assay, the viral multiplication was detected by the immunofluorescence, the cell apoptosis after virus infection was detected by FCM and the level of IFN-β was analyzed by ELISA. Compared to the wild group, the expression level of p53 in the interference group decreased significantly, which indicated that the HepG2 cell strain with the low expression level of p53 was successfully built. 24h after DV infection, the virus titration in the interference group was 100 times higher than that in the wild group. The result of the immunofluorescence showed that, the amount of green fluorescent cells in the interference group was significant higher than that in the wild group. It was indicated that the DV infection was inhibited by p53. However, 24h after DV infection, there was no significant difference in the amount of apoptotic cells in both groups. And the amount of IFN-β in the wild group increased 6 times. The DV infection was inhibited by the transcription factor p53 by activating type I interferon pathway other than promoting the cell apoptosis.