The inhibiting effect of the transcription factor p53 on dengue virus infection by activating the type I interferon
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Yan-Ling Hu1, Xiao-Shan Li1, Shu Xiong1, Qiang Ma1, Dan Liu1, Zhong-Quan Shi1, Jing Tang1, Xian-Cai Rao2, Fu-Quan Hu2, Guo-Li Li1
1Department of Pathogen Biology and Immunology, Chongqing Three Gorges Medical College, Chongqing 404120, China
2Department of Microbiology, The Third Military Medical University, Chongqing 400038, China
Guo-Li Li, email: [email protected]
Keywords: dengue virus, p53, apoptosis, interferon, cell apoptosis
Received: November 09, 2016 Accepted: January 11, 2017 Published: February 15, 2017
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.
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