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Dr. Fouad Fouad Saad Elmayet :: Publications:

Title:
Regulation of Krüppel-Like Factor 15 Expression by Herpes Simplex Virus Type 1 or Bovine Herpesvirus 1 Productive Infecti
Authors: Fouad S. El-mayet , Kelly S. Harrison and Clinton Jones
Year: 2021
Keywords: herpes simplex virus type 1 (HSV-1); bovine herpesvirus 1 (BoHV-1); Krüppel-like factor 15 (KLF15); infected cell protein 0 (ICP0); BoHV-1 ICP0 (bICP0)
Journal: Viruses
Volume: 13
Issue: Not Available
Pages: 1148
Publisher: MDPI
Local/International: International
Paper Link:
Full paper Fouad Fouad Saad Elmayet_El-mayet et al., 2021- Viruses.pdf
Supplementary materials Not Available
Abstract:

Expression of Krüppel-like factor 15 (KLF15), a stress-induced transcription factor, is induced during bovine herpesvirus 1 (BoHV-1) reactivation from latency, and KLF15 stimulates BoHV-1 replication. Transient transfection studies revealed that KLF15 and glucocorticoid receptor (GR) cooperatively transactivate the BoHV-1-immediate-early transcription unit 1 (IEtu1), herpes simplex virus type 1 (HSV-1) infected cell protein 0 (ICP0), and ICP4 promoters. The IEtu1 promoter drives expression of bICP0 and bICP4, two key BoHV-1 transcriptional regulatory proteins. Based on these studies, we hypothesized infection is a stressful stimulus that increases KLF15 expression and enhances productive infection. New studies demonstrated that silencing KLF15 impaired HSV-1 productive infection, and KLF15 steady-state protein levels were increased at late stages of productive infection. KLF15 was primarily localized to the nucleus following infection of cultured cells with HSV-1, but not BoHV-1. When cells were transfected with a KLF15 promoter construct and then infected with HSV-1, promoter activity was significantly increased. The ICP0 gene, and to a lesser extent, bICP0 transactivated the KLF15 promoter in the absence of other viral proteins. In contrast, BoHV-1 or HSV-1 encoded VP16 had no effect on KLF15 promoter activity. Collectively, these studies revealed that HSV-1 and BoHV-1 productive infection increased KLF15 steady-state protein levels, which correlated with increased virus production.

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