HSV-1 ICP27 suppresses NF-κB activity by stabilizing IκBα

Abstract 

Nuclear factor κB (NF-κB) is associated with the transcriptional activation of genes encoding chemokines, adhesion molecules, cytokines, and anti-apoptotic proteins, which are key components in immune responses and viral infection. Many viruses modulate NF-κB through numerous viral gene products to allow productive infections and immune escape. Here we report that herpes simplex virus-1 infected cell protein 27 (HSV-1 ICP27), an immediate early protein of HSV-1, represses NF-κB activity through binding to inhibitor of κB (IκBα), blocking phosphorylation and ubiquitination of IκBα, and stabilizing IκBα. These data may explain how NF-κB activity is regulated by ICP27 to escape immune responses during the very early period of HSV-1 infection.

Structured summary

Abbreviations: NF-κB, nuclear factor κB, HSV-1 ICP27, herpes simplex virus-1 infected cell proteins 27, EMSA, electrophoretic mobility shift assay, IKK, IκB kinase, CHX, cycloheximide

Keywords: NF-κB, HSV-1, HSV-1 ICP27, IκBα