Bovine Herpesvirus 2 Infections

Author(s):  
F. M. M. Scott
Keyword(s):  
1987 ◽  
Vol 61 (12) ◽  
pp. 4023-4025 ◽  
Author(s):  
L J Bello ◽  
J C Whitbeck ◽  
W C Lawrence

1989 ◽  
Vol 63 (4) ◽  
pp. 1525-1530 ◽  
Author(s):  
J J Carter ◽  
A D Weinberg ◽  
A Pollard ◽  
R Reeves ◽  
J A Magnuson ◽  
...  

1991 ◽  
Vol 65 (2) ◽  
pp. 621-631 ◽  
Author(s):  
I Rauh ◽  
F Weiland ◽  
F Fehler ◽  
G M Keil ◽  
T C Mettenleiter

2003 ◽  
Vol 65 (1) ◽  
pp. 87-93 ◽  
Author(s):  
Akihiro ASANO ◽  
Yasuo INOSHIMA ◽  
Kenji MURAKAMI ◽  
Yuko IKETANI ◽  
Yasunori YAMAMOTO ◽  
...  

1982 ◽  
Vol 23 (4) ◽  
pp. 565-569
Author(s):  
C. Ek-Kommonen ◽  
P. Veijalainen ◽  
M. Rantala ◽  
E. Neuvonen

Viruses ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1148
Author(s):  
Fouad S. El-mayet ◽  
Kelly S. Harrison ◽  
Clinton Jones

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.


Immunology ◽  
2004 ◽  
Vol 112 (2) ◽  
pp. 328-338 ◽  
Author(s):  
Sharmila Manoj ◽  
Philip J. Griebel ◽  
Lorne A. Babiuk ◽  
Sylvia Van Drunen Littel-Van Den Hurk

2017 ◽  
Vol 28 (4) ◽  
pp. 248-252 ◽  
Author(s):  
Sachin S. Pawar ◽  
Chetan D. Meshram ◽  
Niraj K. Singh ◽  
Mohini Saini ◽  
B. P. Mishra ◽  
...  

Reproduction ◽  
2007 ◽  
Vol 134 (1) ◽  
pp. 183-197 ◽  
Author(s):  
Gaetano Donofrio ◽  
Shan Herath ◽  
Chiara Sartori ◽  
Sandro Cavirani ◽  
Cesidio Filippo Flammini ◽  
...  

Bovinepostpartumuterine disease, metritis, affects about 40% of animals and is widely considered to have a bacterial aetiology. Although the γ-herpesvirus bovine herpesvirus 4 (BoHV-4) has been isolated from several outbreaks of metritis or abortion, the role of viruses in endometrial pathology and the mechanisms of viral infection of uterine cells are often ignored. The objectives of the present study were to explore the interaction, tropism and outcomes of BoHV-4 challenge of endometrial stromal and epithelial cells. Endometrial stromal and epithelial cells were purified and infected with a recombinant BoHV-4 carrying an enhanced green fluorescent protein (EGFP) expression cassette to monitor the establishment of infection. BoHV-4 efficiently infected both stromal and epithelial cells, causing a strong non-apoptotic cytopathic effect, associated with robust viral replication. The crucial step for the BoHV-4 endometriotropism appeared to be after viral entry as there was enhanced transactivation of the BoHV-4 immediate early 2 gene promoter following transient transfection into the endometrial cells. Infection with BoHV-4 increased cyclooxygenase 2 protein expression and prostaglandin estradiol secretion in endometrial stromal cells, but not epithelial cells. Bovine macrophages are persistently infected with BoHV-4, and co-culture with endometrial stromal cells reactivated BoHV-4 replication in the persistently infected macrophages, suggesting a symbiotic relationship between the cells and virus. In conclusion, the present study provides evidence of cellular and molecular mechanisms, supporting the concept that BoHV-4 is a pathogen associated with uterine disease.


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