scholarly journals Bovine herpesvirus 1-induced apoptosis: phenotypic characterization of susceptible peripheral blood mononuclear cells

1998 ◽  
Vol 143 (3) ◽  
pp. 441-452 ◽  
Author(s):  
E. Hanon ◽  
M. Lambot ◽  
S. Hoornaert ◽  
J. Lyaku ◽  
P. P. Pastoret
Keyword(s):  
Peripheral Blood Mononuclear Cells ◽  
Mononuclear Cells ◽  
Bovine Herpesvirus ◽  
Phenotypic Characterization ◽  
Peripheral Blood Mononuclear ◽  
Bovine Herpesvirus 1 ◽  
Blood Mononuclear Cells ◽  
Herpesvirus 1 ◽  
Induced Apoptosis

scholarly journals Activation of Caspases and p53 by Bovine Herpesvirus 1 Infection Results in Programmed Cell Death and Efficient Virus Release

1999 ◽  
Vol 73 (5) ◽  
pp. 3778-3788 ◽  
Author(s):  
Laxminarayana R. Devireddy ◽  
Clinton J. Jones
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Peripheral Blood Mononuclear Cells ◽  
Mononuclear Cells ◽  
Bovine Herpesvirus ◽  
Virus Release ◽  
Peripheral Blood Mononuclear ◽  
Bovine Herpesvirus 1 ◽  
Blood Mononuclear Cells ◽  
Herpesvirus 1

ABSTRACT Programmed cell death (PCD), or apoptosis, is initiated in response to various stimuli, including virus infection. Bovine herpesvirus 1 (BHV-1) induces PCD in peripheral blood mononuclear cells at the G0/G1 phase of the cell cycle (E. Hanon, S. Hoornaert, F. Dequiedt, A. Vanderplasschen, J. Lyaku, L. Willems, and P.-P. Pastoret, Virology 232:351–358, 1997). However, penetration of virus particles is not required for PCD (E. Hanon, G. Meyer, A. Vanderplasschen, C. Dessy-Doize, E. Thiry, and P. P. Pastoret, J. Virol. 72:7638–7641, 1998). The mechanism by which BHV-1 induces PCD in peripheral blood mononuclear cells is not understood, nor is it clear whether nonlymphoid cells undergo PCD following infection. This study demonstrates that infection of bovine kidney (MDBK) cells with BHV-1 leads to PCD, as judged by terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling, DNA laddering, and chromatin condensation. p53 appears to be important in this process, because p53 levels and promoter activity increased after infection. Expression of proteins that are stimulated by p53 (p21Waf1 and Bax) is also activated after infection. Cleavage of Bcl-xL, a protein that inhibits PCD, occurred after infection, suggesting that caspases (interleukin-1β-converting enzyme-like proteases) were activated. Other caspase substrates [poly(ADP-ribose) polymerase and actin] are also cleaved during the late stages of infection. Inhibition of caspase activity delayed cytotoxic activity and virus release but increased the overall virus yield. Taken together, these results indicate that nonlymphoid cells undergo PCD near the end of productive infection and further suggest that caspases enhance virus release.

scholarly journals Transcriptomic Profiling of Equine and Viral Genes in Peripheral Blood Mononuclear Cells in Horses during Equine Herpesvirus 1 Infection

Pathogens ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 43
Author(s):  
Lila M. Zarski ◽  
Patty Sue D. Weber ◽  
Yao Lee ◽  
Gisela Soboll Hussey
Keyword(s):  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Differentially Expressed ◽  
Equine Herpesvirus ◽  
Peripheral Blood Mononuclear ◽  
Equine Herpesvirus 1 ◽  
Blood Mononuclear Cells ◽  
Herpesvirus 1

Equine herpesvirus 1 (EHV-1) affects horses worldwide and causes respiratory disease, abortions, and equine herpesvirus myeloencephalopathy (EHM). Following infection, a cell-associated viremia is established in the peripheral blood mononuclear cells (PBMCs). This viremia is essential for transport of EHV-1 to secondary infection sites where subsequent immunopathology results in diseases such as abortion or EHM. Because of the central role of PBMCs in EHV-1 pathogenesis, our goal was to establish a gene expression analysis of host and equine herpesvirus genes during EHV-1 viremia using RNA sequencing. When comparing transcriptomes of PBMCs during peak viremia to those prior to EHV-1 infection, we found 51 differentially expressed equine genes (48 upregulated and 3 downregulated). After gene ontology analysis, processes such as the interferon defense response, response to chemokines, the complement protein activation cascade, cell adhesion, and coagulation were overrepresented during viremia. Additionally, transcripts for EHV-1, EHV-2, and EHV-5 were identified in pre- and post-EHV-1-infection samples. Looking at micro RNAs (miRNAs), 278 known equine miRNAs and 855 potentially novel equine miRNAs were identified in addition to 57 and 41 potentially novel miRNAs that mapped to the EHV-2 and EHV-5 genomes, respectively. Of those, 1 EHV-5 and 4 equine miRNAs were differentially expressed in PBMCs during viremia. In conclusion, this work expands our current knowledge about the role of PBMCs during EHV-1 viremia and will inform the focus on future experiments to identify host and viral factors that contribute to clinical EHM.

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