scholarly journals Ultrastructure and immuno-cytochemistry of BHK-21 cells infected with a modified Bucyrus strain of equine arteritis virus

1995 ◽  
Vol 140 (7) ◽  
pp. 1173-1180 ◽  
Author(s):  
R. Wada ◽  
Y. Fukunaga ◽  
T. Kondo ◽  
T. Kanemaru
2012 ◽  
Vol 32 (8) ◽  
pp. 479-480
Author(s):  
J.R. Campos ◽  
M.H.T. Troedsson ◽  
P. Breheny ◽  
R.R. Araujo ◽  
E.L. Squires ◽  
...  

Intervirology ◽  
2011 ◽  
Vol 54 (1) ◽  
pp. 30-36 ◽  
Author(s):  
Germán Ernesto Metz ◽  
Giselle Paula Martín Ocampos ◽  
María Soledad Serena ◽  
Sabrina Eliana Gambaro ◽  
Edgardo Nosetto ◽  
...  

Author(s):  
J.T. Paweska ◽  
M.M. Henton ◽  
J.J. Van der Lugt

Clinical, virological and serological responses were evaluated in 10 pregnant mares after different challenge exposures to the asinine-94 strain of equine arteritis virus (EAV). The outcome of maternal infection on the progeny was also investigated. Mares were inoculated intranasally (n = 4), intramuscularly (n = 2), intravenously (n = 1), or contact-exposed (n = 3). All inoculated mares developed pyrexia, 5 showed mild clinical signs related to EAV infection and 2 remained asymptomatic. Viraemia was detected in all the inoculated animals and shedding of virus from the respiratory tract occurred in 6. Five mares were re-challenged intranasally 7 and 15 weeks after inoculation. Clinical signs of the disease in these mares were limited to mild conjunctivitis. After re-challenge, virus was recovered from buffy coat cultures of 2 mares 2-6 days after re-infection. EAV was not recovered from colostrum and milk samples during the 1st week post partum. All inoculated mares seroconverted to EAV 8-12 days post inoculation and also seroconverted after re-challenge. No clinical signs of EAV infection were observed in the 3 mares kept in close contact during the post-inoculation and re-challenge periods. Serum neutralising antibody to the virus was detected in 1 in-contact mare only, while a detectable concentration of specific IgG was found by ELISA in the colostrum of 1 of the other in-contact mares. Eight of the mares gave birth to clinically normal foals, although 1 was born prematurely. Shortly after birth, 7 foals developed fever and variable clinical signs; 5 foals became septicaemic and 3 of them died 2-5 days after birth, while the remaining 2 were euthanased at 1 month of age. EAV was not recovered from the placenta, from buffy coat fractions of blood collected from foals immediately after birth and 1-3 days later, or from a range of tissues taken from the 3 foals that died and 2 that were euthanased. Virus was not isolated from tissues collected from 1 mare and her foetus 3 weeks after this mare was re-challenged.


Author(s):  
Jodi Hedges ◽  
Udeni B. R. Balasuriya ◽  
Jb Topol ◽  
Dustin W. Lee ◽  
N. James Maclachlan

2004 ◽  
Vol 85 (12) ◽  
pp. 3709-3714 ◽  
Author(s):  
Jessika C. Zevenhoven-Dobbe ◽  
Sophie Greve ◽  
Hans van Tol ◽  
Willy J. M. Spaan ◽  
Eric J. Snijder

2001 ◽  
Vol 82 (10) ◽  
pp. 2425-2435 ◽  
Author(s):  
J. Castillo-Olivares ◽  
A. A. F. de Vries ◽  
M. J. B. Raamsman ◽  
P. J. M. Rottier ◽  
K. Lakhani ◽  
...  

An Escherichia coli-expressed recombinant protein (6hisGLecto) comprising the entire ectodomain (aa 18–122) of equine arteritis virus (EAV) glycoprotein GL, the immunodominant viral antigen, induced higher neutralizing antibody titres than other GL-derived polypeptides when compared in an immunization study in ponies. The potential of the recombinant GL ectodomain to act as a sub-unit vaccine against EAV was evaluated further in three groups of four ponies vaccinated with doses of 35, 70 or 140 μg of protein. All vaccinated animals developed a virus-neutralizing antibody (VNAb) response with peak titres 1–2 weeks after the administration of a booster on week 5 (VNAb titres of 1·8–3·1), 13 (VNAb titres of 1·4–2·9) or 53 (VNAb titres of 1·2–2·3). Vaccinated and unvaccinated control ponies were infected with EAV at different times post-vaccination to obtain information about the degree of protection relative to the levels of pre-challenge VNAb. Vaccination conferred varying levels of protection, as indicated by reduced or absent pyrexia, viraemia and virus excretion from the nasopharynx. The degree of protection correlated well with the levels of pre-challenge VNAb and, in particular, with levels of virus excretion. These results provide the first evidence that a sub-unit vaccine protects horses against EAV. The use of the sub-unit vaccine in combination with a differential diagnostic test based on other EAV antigens would enable serological discrimination between naturally infected and vaccinated equines.


2019 ◽  
Vol 93 (12) ◽  
Author(s):  
Jiyao Chen ◽  
Dang Wang ◽  
Zheng Sun ◽  
Li Gao ◽  
Xinyu Zhu ◽  
...  

ABSTRACTEquine arteritis virus (EAV) and porcine reproductive and respiratory syndrome virus (PRRSV) represent two members of the familyArteriviridaeand pose major threats for the horse- and swine-breeding industries worldwide. A previous study suggested that PRRSV nsp4, a 3C-like protease, antagonizes interferon beta (IFN-β) production by cleaving the NF-κB essential modulator (NEMO) at a single site, glutamate 349 (E349). Here, we demonstrated that EAV nsp4 also inhibited virus-induced IFN-β production by targeting NEMO for proteolytic cleavage and that the scission occurred at four sites: E166, E171, glutamine 205 (Q205), and E349. Additionally, we found that, besides the previously reported cleavage site E349 in NEMO, scission by PRRSV nsp4 took place at two additional sites, E166 and E171. These results imply that while cleaving NEMO is a common strategy utilized by EAV and PRRSV nsp4 to antagonize IFN induction, EAV nsp4 adopts a more complex substrate recognition mechanism to target NEMO. By analyzing the abilities of the eight different NEMO fragments resulting from EAV or PRRSV nsp4 scission to induce IFN-β production, we serendipitously found that a NEMO fragment (residues 1 to 349) could activate IFN-β transcription more robustly than full-length NEMO, whereas all other NEMO cleavage products were abrogated for the IFN-β-inducing capacity. Thus, NEMO cleavage at E349 alone may not be sufficient to completely inactivate the IFN response via this signaling adaptor. Altogether, our findings suggest that EAV and PRRSV nsp4 cleave NEMO at multiple sites and that this strategy is critical for disarming the innate immune response for viral survival.IMPORTANCEThe arterivirus nsp4-encoded 3C-like protease (3CLpro) plays an important role in virus replication and immune evasion, making it an attractive target for antiviral therapeutics. Previous work suggested that PRRSV nsp4 suppresses type I IFN production by cleaving NEMO at a single site. In contrast, the present study demonstrates that both EAV and PRRSV nsp4 cleave NEMO at multiple sites and that this strategy is essential for disruption of type I IFN production. Moreover, we reveal that EAV nsp4 also cleaves NEMO at glutamine 205 (Q205), which is not targeted by PRRSV nsp4. Notably, targeting a glutamine in NEMO for cleavage has been observed only with picornavirus 3C proteases (3Cpro) and coronavirus 3CLpro. In aggregate, our work expands knowledge of the innate immune evasion mechanisms associated with NEMO cleavage by arterivirus nsp4 and describes a novel substrate recognition characteristic of EAV nsp4.


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