Loading…

Inhibition of Nuclear Factor κB Activation by a Virus-encoded IκB-like Protein

Certain viruses have evolved mechanisms to counteract innate immunity, a host response in which nuclear factor Kappa B (NF- Kappa B) transcription factors play a central role. African swine fever virus encodes a protein of 28.2 kDa containing ankyrin repeats similar to those of cellular I Kappa B pr...

Full description

Saved in:
Bibliographic Details
Published in:The Journal of biological chemistry 1998-02, Vol.273 (9), p.5405-5411
Main Authors: Revilla, Yolanda, Callejo, Mario, Rodrı́guez, Javier M., Culebras, Esther, Nogal, Marı́a L., Salas, Marı́a L., Viñuela, Eladio, Fresno, Manuel
Format: Article
Language:English
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Certain viruses have evolved mechanisms to counteract innate immunity, a host response in which nuclear factor Kappa B (NF- Kappa B) transcription factors play a central role. African swine fever virus encodes a protein of 28.2 kDa containing ankyrin repeats similar to those of cellular I Kappa B proteins, which are inhibitors of NF- Kappa B. Transfection of the African swine fever virus I Kappa B gene inhibited tumor necrosis factor- or phorbol ester-induced activation of Kappa B- but not AP-1-driven reporter genes. Moreover, African swine fever virus I Kappa B co-immunoprecipitated with p65 NF- Kappa B, and the purified recombinant protein prevented the binding of p65-p50 NF- Kappa B proteins to their target sequences in the DNA. NF- Kappa B activation induced by tumor necrosis factor, as detected by mobility shift assays or by transfection of Kappa B-driven reporter genes, is impaired in African swine fever virus-infected cells. These results indicate that the African swine fever virus I Kappa B gene homologue interferes with NF- Kappa B activation, likely representing a new mechanism to evade the immune response during viral infection.
ISSN:0021-9258
DOI:10.1074/jbc.273.9.5405