scholarly journals Regulation of Innate Immune Responses by Bovine Herpesvirus 1 and Infected Cell Protein 0 (bICP0)

Viruses ◽  
2009 ◽  
Vol 1 (2) ◽  
pp. 255-275 ◽  
Author(s):  
Clinton Jones
Keyword(s):  
Immune Responses ◽  
Infected Cell ◽  
Bovine Herpesvirus ◽  
Innate Immune ◽  
Cell Protein ◽  
Innate Immune Responses ◽  
Bovine Herpesvirus 1 ◽  
Infected Cell Protein ◽  
Herpesvirus 1 ◽  
Infected Cell Protein 0

A pioneer transcription factor and type I nuclear hormone receptors synergistically activate the bovine herpesvirus 1 infected cell protein 0 (ICP0) early promoter.

2021 ◽  
Author(s):  
Laximan Sawant ◽  
Jeffery B. Ostler ◽  
Clinton Jones
Keyword(s):  
Infected Cell ◽  
Binding Sites ◽  
Cell Protein ◽  
Type I ◽  
Bovine Herpesvirus 1 ◽  
Early Promoter ◽  
Infected Cell Protein ◽  
Herpesvirus 1 ◽  
Pioneer Transcription Factor ◽  
Infected Cell Protein 0

Following bovine herpesvirus 1 (BoHV-1) acute infection of ocular, oral or nasal cavities, sensory neurons within trigeminal ganglia are an important site for latency. Stress, as mimicked by the synthetic corticosteroid dexamethasone, consistently induces reactivation from latency. Expression of two key viral transcriptional regulatory proteins, infected cell protein 0 (bICP0) and bICP4, are regulated by sequences within the immediate early promoter (IEtu1). A separate early promoter also drives bICP0 expression, presumably to ensure sufficient levels of this important transcriptional regulatory protein. Productive infection and bICP0 early promoter activity are cooperatively transactivated by Krüppel like factor 4 (KLF4) and a Type I nuclear hormone receptor (NHR), androgen receptor, glucocorticoid receptor, or progesterone receptor. The bICP0 early promoter contains 3 separate transcriptional enhancers that mediate cooperative transactivation. In contrast to the IEtu1 promoter, the bICP0 early promoter lacks consensus Type I NHR binding sites. Consequently, we hypothesized KLF4 and Sp1 binding sites are essential for Type I NHR and KLF4 to transactivate the bICP0 promoter. Mutating KLF4 and Sp1 binding sites in each enhancer domain significantly reduced transactivation by KLF4 and a Type I NHR. Chromatin immunoprecipitation (ChIP) studies demonstrated occupancy of bICP0 early promoter sequences by KLF4 and Type I NHR is significantly reduced when KLF4 and/or Sp1 binding sites were mutated. These studies suggest cooperative transactivation of the bICP0 E promoter by Type I NHRs and a stress induced pioneer transcription factor (KLF4) promote viral replication and spread in neurons or non-neural cells in reproductive tissue. IMPORTANCE Understanding how stressful stimuli and changes in cellular milieu mediate viral replication and gene expression in the natural host is important for developing therapeutic strategies that impair virus transmission and disease. For example, bovine herpesvirus 1 (BoHV-1) reactivation from latency is consistently induced by the synthetic corticosteroid dexamethasone, which mimics the effects of stress. Furthermore, BoHV-1 infection increases the incidence of abortion in pregnant cows suggesting sex hormones stimulate viral growth in certain tissue. Previous studies revealed Type I nuclear hormone receptors (androgen, glucocorticoid, or progesterone) and the pioneer transcription factor, Krüppel like factor 4 (KLF4), cooperatively transactivate the BoHV-1 infected cell protein 0 (bICP0) early promoter. Transactivation was mediated by Sp1 and/or KLF4 consensus binding sites within the 3 transcriptional enhancers. These studies underscore the complexity by which BoHV-1 exploits Type I NHR fluctuations to enhance viral gene expression, replication, and transmission in the natural host.

Stimulation of Innate Immune Responses by CpG Oligodeoxynucleotide in Newborn Lambs Can Reduce Bovine Herpesvirus-1 Shedding

2006 ◽  
Vol 16 (1) ◽  
pp. 58-67 ◽  
Author(s):  
Anil K. Nichani ◽  
Angelo Mena ◽  
Radhey S. Kaushik ◽  
George K. Mutwiri ◽  
Hugh G.G. Townsend ◽  
...  
Keyword(s):  
Immune Responses ◽  
Bovine Herpesvirus ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Bovine Herpesvirus 1 ◽  
Cpg Oligodeoxynucleotide ◽  
Herpesvirus 1 ◽  
Stimulation Of

scholarly journals The bovine herpesvirus 1 gene encoding infected cell protein 0 (bICP0) can inhibit interferon-dependent transcription in the absence of other viral genes

2005 ◽  
Vol 86 (10) ◽  
pp. 2697-2702 ◽  
Author(s):  
Gail Henderson ◽  
Yange Zhang ◽  
Clinton Jones
Keyword(s):  
Gene Expression ◽  
Ring Finger ◽  
Viral Gene Expression ◽  
Bovine Herpesvirus ◽  
Productive Infection ◽  
Cell Protein ◽  
Viral Gene ◽  
Bovine Herpesvirus 1 ◽  
Infected Cell Protein ◽  
Herpesvirus 1

The infected cell protein 0 (bICP0) encoded by Bovine herpesvirus 1 (BHV-1) stimulates viral gene expression and productive infection. As bICP0 is expressed constitutively during productive infection, it is considered to be the major viral regulatory protein. Like other alphaherpesvirus ICP0 homologues, bICP0 contains a zinc RING finger near its N terminus that activates transcription and regulates subcellular localization. In this study, evidence is provided that bICP0 represses the human beta interferon (IFN-β) promoter and a simple promoter with consensus IFN-stimulated response elements following stimulation with double-stranded RNA (polyinosinic–polycytidylic acid), IFN regulatory factor 3 (IRF3) or IRF7. bICP0 also inhibits the ability of two protein kinases (TBK1 and IKKε) to activate IFN-β promoter activity. The zinc RING finger is necessary for inhibiting IFN-dependent transcription in certain cell types. Collectively, these studies suggest that bICP0 activates productive infection by stimulating viral gene expression and inhibiting IFN-dependent transcription.

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