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

Nuclear factor kappa B (NF-kappa B) 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-kappa B 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-kappa B activity through binding to inhibitor of kappa B (I kappa B alpha), blocking phosphorylation and ubiquitination of I kappa B alpha, and stabilizing I kappa B alpha. These data may explain how NF-kappa B activity is regulated by ICP27 to escape immune responses during the very early period of HSV-1 infection.