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

Li Ding1, Jiawei Li1, Weihao Li1

  • 1Ministry of Education Key Laboratory for Ecology of Tropical Islands, College of Life Sciences, Hainan Normal University, Haikou, Hainan, 571158, China.

Veterinary Microbiology
|November 27, 2018
PubMed

Insights

The tumor suppressor p53 protein helps control Transmissible Gastroenteritis Virus (TGEV) replication by boosting interferon-beta (IFN-β) signaling. Loss of p53 impairs this antiviral response, leading to increased virus levels.

Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • Transmissible Gastroenteritis Virus (TGEV) infection triggers interferon-beta (IFN-β) production, crucial for antiviral immunity.
  • Previous research indicated TGEV activates p53 signaling, inducing apoptosis that may affect viral replication.
  • The interplay between p53 and IFN-β signaling during TGEV infection remained uncharacterized.

Purpose of the Study:

  • To investigate the role of p53 in modulating IFN-β signaling and TGEV replication.
  • To compare TGEV infection outcomes in p53 wild-type and p53-deficient cells.

Main Methods:

  • Infection of p53 wild-type (WT PK-15) and p53-deficient (p53-/- PK-15) cells with a low dose of TGEV.
  • Analysis of IFN-β expression and production.
  • Quantification of mRNA levels for key interferon pathway genes (TRIF, TRAM, MDA5, RIG-I, IPS-1, IRF9, IRF3, ISG15, ISG20).
  • Measurement of TGEV genomic RNA and subgenomic mRNA (N gene, ORF7).
  • Determination of viral titers.
  • Treatment with exogenous IFN-β and polyinosinic-polycytidylic acid (poly(I:C)).

Main Results:

  • IFN-β expression and production were significantly reduced in p53-/- PK-15 cells early in TGEV infection.
  • TGEV-induced changes in key interferon pathway gene mRNA levels were hindered in p53-/- PK-15 cells.
  • Increased levels of TGEV genomic RNA and specific viral mRNAs (N, ORF7) were observed in p53-/- PK-15 cells.
  • Viral titers were notably higher in p53-/- PK-15 cells compared to WT PK-15 cells.
  • Exogenous IFN-β and poly(I:C) treatment inhibited TGEV replication in both cell types.

Conclusions:

  • p53 plays a critical role in mediating IFN-β signaling to restrict TGEV replication during the early stages of infection.
  • The p53-dependent IFN-β pathway is essential for controlling TGEV proliferation.
Keywords:
IFN-βTGEVViral replicationp53

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