Differential Regulation of NF-kappaB Signaling during Human Cytomegalovirus Infection.
10.4167/jbv.2015.45.2.159
- Author:
Ki Mun KWON
1
;
Jin Hyun AHN
Author Information
1. Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Suwon, Korea. jahn@skku.edu
- Publication Type:Review
- Keywords:
Cytomegalovirus;
NF-kappaB;
Immune response;
Tegument protein
- MeSH:
Apoptosis;
Cytomegalovirus;
Cytomegalovirus Infections*;
DNA;
Genes, Viral;
Humans;
Immunity, Innate;
Inflammation;
NF-kappa B*;
Receptors, Tumor Necrosis Factor;
Transcription Factors
- From:Journal of Bacteriology and Virology
2015;45(2):159-164
- CountryRepublic of Korea
- Language:English
-
Abstract:
NF-kappaB transcription factors are key regulators of immune and stress responses, apoptosis, and differentiation. Human cytomegalovirus (HCMV) activates or represses NF-kappaB signaling at different times during infection. An initial increase in NF-kappaB activity occurs within a few hours of infection. The virus appears to adapt to this change since initial viral gene expression is promoted by the elevated NF-kappaB activity. Because NF-kappaB upregulates innate immune responses and inflammation, it has also been suggested that HCMV needs to downregulate NF-kappaB signaling. Recent studies have shown that HCMV has various mechanisms that inhibit NF-kappaB signaling. HCMV reduces cell surface expression of tumor necrosis factor receptor 1 (TNFR1) and blocks the DNA binding activity of NF-kappaB. Furthermore, some HCMV tegument proteins antagonize NF-kappaB activation by targeting the key components of NF-kappaB signaling at late stages of infection. In this review, we summarize the recent findings on the relationship between HCMV and NF-kappaB signaling, focusing, in particular, on the viral mechanisms by which the NF-kappaB signaling pathway is inhibited.
