1. Academic Validation
  2. p53 mediated IFN-β signaling to affect viral replication upon TGEV infection

p53 mediated IFN-β signaling to affect viral replication upon TGEV infection

  • Vet Microbiol. 2018 Dec;227:61-68. doi: 10.1016/j.vetmic.2018.10.025.
Li Ding 1 Jiawei Li 1 Weihao Li 1 Zhenhua Fang 2 Na Li 1 Qiqi Guo 1 Haoyue Qu 1 Dan Feng 1 Jiangyue Li 1 Meiling Hong 3
Affiliations

Affiliations

  • 1 Ministry of Education Key Laboratory for Ecology of Tropical Islands, College of Life Sciences, Hainan Normal University, Haikou, Hainan, 571158, China.
  • 2 School of Tropical Agricultural Technology, Hainan College of Vocation and Technique, Haikou, Hainan, 570216, China.
  • 3 Ministry of Education Key Laboratory for Ecology of Tropical Islands, College of Life Sciences, Hainan Normal University, Haikou, Hainan, 571158, China. Electronic address: mlhong@hainnu.edu.cn.
Abstract

TGEV can induce IFN-β production, which in turn plays a vital role in host Antiviral immune responses. Our previous studies showed that TGEV Infection activated p53 signaling to induce host cell Apoptosis, which might influence virus replication. However, whether there be an interaction between p53 and IFN-β signaling in the process of TGEV Infection is unknown. In the present study, we used low dose of TGEV to infect p53 wild-type PK-15 cells (WT PK-15 cells) and p53 deficient cells (p53-/- PK-15 cells), to investigate the modulation of IFN signaling and virus replication by p53. The results showed that the IFN-β expression and production were notably inhibited in p53-/- PK-15 cells compared with that in WT PK-15 cells at early stage of TGEV Infection. In addition, TGEV-induced the changes in mRNA levels of TRIF, TRAM, MDA5, RIG-I, IPS-1, IRF9, IRF3, ISG15 and ISG20 were notably hindered in p53-/- PK-15 cells before 36 h post Infection (p.i.). Moreover, TGEV genomic RNA and sub genomic mRNA (N gene and ORF7) levels showed significant increase in p53-/- PK-15 cells compared with WT PK-15 cells after TGEV Infection. And viral titers were observably enhanced in p53-/- PK-15 cells. Furthermore, exogenous IFN-β and polyinosinic-polycytidylic acid (poly (I:C)) treatment markedly inhibited the mRNA levels of TGEV gRNA, N and ORF7 in WT PK-15 cells and p53-/- PK-15 cells compared to control. Taken together, these results demonstrated that p53 may mediate IFN-β signaling to inhibit viral replication early after TGEV Infection.

Keywords

IFN-β; TGEV; Viral replication; p53.

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