scholarly journals Effect of tunicamycin and monensin on fusion and hemadsorptive activities of equid herpesvirus 1.

1991 ◽  
Vol 53 (1) ◽  
pp. 133-135
Author(s):  
Nobuo KOIZUMI ◽  
Eiichi HONDA ◽  
Tetsuo KUMAGAI ◽  
Katsunori OKAZAKI
Keyword(s):  
Equid Herpesvirus ◽  
Herpesvirus 1

scholarly journals Equid Herpesvirus 1 Infection in Mice.

1993 ◽  
Vol 55 (1) ◽  
pp. 119-121 ◽  
Author(s):  
Mamiko INAZU ◽  
Osamu TSUHA ◽  
Rikio KIRISAWA ◽  
Yoshimi KAWAKAMI ◽  
Hiroshi IWAI
Keyword(s):  
Equid Herpesvirus ◽  
Herpesvirus 1

Replication of equid herpesvirus-1 (EHV-1) in the testes and epididymides of ponies and venereal shedding of infectious virus

1996 ◽  
Vol 115 (4) ◽  
pp. 385-397 ◽  
Author(s):  
J.P. Tearle ◽  
K.C. Smith ◽  
M.S. Boyle ◽  
M.M. Binns ◽  
G.J. Livesay ◽  
...  
Keyword(s):  
Infectious Virus ◽  
Equid Herpesvirus ◽  
Herpesvirus 1

Trials of an inactivated equid herpesvirus 1 vaccine: challenge with a subtype 1 virus

1984 ◽  
Vol 114 (15) ◽  
pp. 369-374 ◽  
Author(s):  
R. Burrows ◽  
D. Goodridge ◽  
M. Denyer
Keyword(s):  
Equid Herpesvirus ◽  
Herpesvirus 1

scholarly journals Equid Herpesvirus 1 Targets the Sensitization and Induction Steps To Inhibit the Type I Interferon Response in Equine Endothelial Cells

2019 ◽  
Vol 93 (23) ◽  
Author(s):  
Fatai S. Oladunni ◽  
Sanjay Sarkar ◽  
Stephanie Reedy ◽  
Udeni B. R. Balasuriya ◽  
David W. Horohov ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cellular Level ◽  
Immune Defense ◽  
Interferon Response ◽  
Type I ◽  
Type I Ifn ◽  
Viral Pathogen ◽  
Equid Herpesvirus ◽  
Herpesvirus 1

ABSTRACT Equid herpesvirus 1 (EHV-1) is a viral pathogen of horse populations worldwide spread by the respiratory route and is known for causing outbreaks of neurologic syndromes and abortion storms. Previously, we demonstrated that an EHV-1 strain of the neuropathogenic genotype, T953, downregulates the beta interferon (IFN-β) response in vitro in equine endothelial cells (EECs) at 12 h postinfection (hpi). In the present study, we explored the molecular correlates of this inhibition as clues toward an understanding of the mechanism. Data from our study revealed that EHV-1 infection of EECs significantly reduced both Toll-like receptor 3 (TLR3) and TLR4 mRNA expression at 6 hpi and 12 hpi. While EHV-1 was able to significantly reduce IRF9 mRNA at both 6 hpi and 12 hpi, the virus significantly reduced IFN regulatory factor 7 (IRF7) mRNA only at 12 hpi. EHV-1 did not alter the cellular level of Janus-activated kinase 1 (JAK1) at any time point. However, EHV-1 reduced the cellular level of expression of tyrosine kinase 2 (TYK2) at 12 hpi. Downstream of JAK1-TYK2 signaling, EHV-1 blocked the phosphorylation and activation of signal transducer and activator of transcription 2 (STAT2) when coincubated with exogenous IFN, at 12 hpi, although not at 3 or 6 hpi. Immunofluorescence staining revealed that the virus prevented the nuclear translocation of STAT2 molecules, confirming the virus-mediated inhibition of STAT2 activation. The pattern of suppression of phosphorylation of STAT2 by EHV-1 implicated viral late gene expression. These data help illuminate how EHV-1 strategically inhibits the host innate immune defense by limiting steps required for type I IFN sensitization and induction. IMPORTANCE To date, no commercial vaccine label has a claim to be fully protective against the diseases caused by equid herpesvirus 1 (EHV-1), especially the neurologic form. The interferon (IFN) system, of which type I IFN is of great importance, still remains a viable immunotherapeutic option against EHV-1 infection. The type I IFN system has been exploited successfully to treat other viral infections, such as chronic hepatitis B and C in humans. The current state of research on how EHV-1 interferes with the protective effect of type I IFN has indicated transient induction of type I IFN production followed by a rapid shutdown in vitro in equine endothelial cells (EECs). The significance of our study is the identification of certain steps in the type I IFN signaling pathway targeted for inhibition by EHV-1. Understanding this pathogen-host relationship is essential for the long-term goal of developing effective immunotherapy against EHV-1.

scholarly journals Zebra-borne neurotropic equid herpesvirus 1 meningoencephalitis in a Thomson’s gazelle (Eudorcas thomsonii)

2017 ◽  
Vol 29 (4) ◽  
pp. 548-556 ◽  
Author(s):  
Kanako Sakaguchi ◽  
Kenneth Kim ◽  
Ingeborg Langohr ◽  
Annabel G. Wise ◽  
Roger K. Maes ◽  
...  
Keyword(s):  
Inclusion Bodies ◽  
Gene Sequence ◽  
Molecular Detection ◽  
Specific Primer ◽  
Molecular Features ◽  
Equid Herpesvirus ◽  
Glycoprotein G ◽  
Microscopic Evaluation ◽  
Antigen Localization ◽  
Herpesvirus 1

We describe the histopathologic, immunohistochemical, and molecular features of a case of meningoencephalitis in a Thomson’s gazelle ( Eudorcas thomsonii) naturally infected with zebra-borne equid herpesvirus 1 (EHV-1) and the implications for the molecular detection of zebra-borne EHV-1. A 4-y-old female Thomson’s gazelle was submitted for postmortem examination; no gross abnormalities were noted except for meningeal congestion. Microscopic evaluation demonstrated multifocal nonsuppurative meningoencephalitis with intranuclear eosinophilic and amphophilic inclusion bodies and EHV-9 antigen in neurons. PCR demonstrated the presence of a herpesvirus with a nucleotide sequence 99–100% identical to the corresponding sequences of zebra-borne EHV-1 and of EHV-9 strains. To determine whether EHV-1 or EHV-9 was involved, a PCR with a specific primer set for EHV-9 ORF59/60 was used. The sequence was identical to that of 3 recognized zebra-borne EHV-1 strains and 91% similar to that of EHV-9. This isolate was designated as strain LM2014. The partial glycoprotein G ( gG) gene sequence of LM2014 was also identical to the sequence of 2 zebra-borne EHV-1 strains (T-529 isolated from an onager, 94-137 from a Thomson’s gazelle). The histologic lesions of encephalitis and antigen localization in this gazelle indicate prominent viral neurotropism, and lesions were very similar to those seen in EHV-1– and EHV-9–infected non-equid species. Histologic lesions caused by EHV-9 and zebra-borne EHV-1 are therefore indistinguishable.

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