Version 1
: Received: 25 May 2021 / Approved: 26 May 2021 / Online: 26 May 2021 (15:10:59 CEST)
How to cite:
El-Mayet, F.S.; Harrison, K.S.; Jones, C. Regulation of Krüppel-like Factor 15 Expression by Herpes Simplex Virus Type 1 or Bovine Herpesvirus 1 Productive Infection. Preprints2021, 2021050648. https://doi.org/10.20944/preprints202105.0648.v1
El-Mayet, F.S.; Harrison, K.S.; Jones, C. Regulation of Krüppel-like Factor 15 Expression by Herpes Simplex Virus Type 1 or Bovine Herpesvirus 1 Productive Infection. Preprints 2021, 2021050648. https://doi.org/10.20944/preprints202105.0648.v1
El-Mayet, F.S.; Harrison, K.S.; Jones, C. Regulation of Krüppel-like Factor 15 Expression by Herpes Simplex Virus Type 1 or Bovine Herpesvirus 1 Productive Infection. Preprints2021, 2021050648. https://doi.org/10.20944/preprints202105.0648.v1
APA Style
El-Mayet, F.S., Harrison, K.S., & Jones, C. (2021). Regulation of Krüppel-like Factor 15 Expression by Herpes Simplex Virus Type 1 or Bovine Herpesvirus 1 Productive Infection. Preprints. https://doi.org/10.20944/preprints202105.0648.v1
Chicago/Turabian Style
El-Mayet, F.S., Kelly S. Harrison and Clinton Jones. 2021 "Regulation of Krüppel-like Factor 15 Expression by Herpes Simplex Virus Type 1 or Bovine Herpesvirus 1 Productive Infection" Preprints. https://doi.org/10.20944/preprints202105.0648.v1
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 KLF15 and glucocorticoid receptor (GR) cooperatively transactivate the BoHV-1 immediate early transcription unit 1 (IEtu1), herpes sim-plex virus type 1 (HSV-1) infected cell protein 0 (ICP0), and ICP4 promoter. 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 ex-pression 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 in-fection 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 pro-moter activity. Collectively, these studies revealed HSV-1 and BoHV-1 productive infection in-creased KLF15 steady state protein levels, which correlated with increased virus production.
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
