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Udeni B.r. Balasuriya - One of the best experts on this subject based on the ideXlab platform.
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Development and Characterization of an Infectious cDNA Clone of Equine Arteritis Virus.
Methods in molecular biology (Clifton N.J.), 2017Co-Authors: Udeni B.r. Balasuriya, Jianqiang ZhangAbstract:Development and characterization of several infectious cDNA clones of Equine Arteritis virus (EAV) have been described in the literature. Here we describe the assembly of the full-length infectious cDNA clone of the virulent Bucyrus strain (VBS; ATCC VR-796) of EAV in a plasmid vector. This system allows generation of infectious in vitro-transcribed (IVT) RNA from the linearized plasmid that can be transfected or electroporated into mammalian cells to produce infectious recombinant progeny virus. This is an efficient reverse genetics system that allows easy manipulation of EAV genomes to study molecular biology of the virus and pathogenesis of Equine Viral Arteritis.
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Equine Viral Arteritis
The Veterinary clinics of North America. Equine practice, 2014Co-Authors: Udeni B.r. BalasuriyaAbstract:Equine Arteritis virus (EAV), the causative agent of Equine Viral Arteritis (EVA), is a respiratory and reproductive disease that occurs throughout the world. EAV infection is highly species-specific and exclusively limited to members of the family Equidae, which includes horses, donkeys, mules, and zebras. EVA is an economically important disease and outbreaks could cause significant losses to the Equine industry. The primary objective of this article is to summarize current understanding of EVA, specifically the disease, pathogenesis, epidemiology, host immune response, vaccination and treatment strategies, prevention and control measures, and future directions.
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Equine Arteritis virus.
Veterinary Microbiology, 2013Co-Authors: Udeni B.r. Balasuriya, N. James MaclachlanAbstract:Equine Arteritis virus (EAV) is the causative agent of Equine Viral Arteritis (EVA), a respiratory and reproductive disease of equids. There has been significant recent progress in understanding the molecular biology of EAV and the pathogenesis of its infection in horses. In particular, the use of contemporary genomic techniques, along with the development and reverse genetic manipulation of infectious cDNA clones of several strains of EAV, has generated significant novel information regarding the basic molecular biology of the virus. Therefore, the objective of this review is to summarize current understanding of EAV virion architecture, replication, evolution, molecular epidemiology and genetic variation, pathogenesis including the influence of host genetics on disease susceptibility, host immune response, and potential vaccination and treatment strategies.
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Emergence of novel Equine Arteritis virus (EAV) variants during persistent infection in the stallion: origin of the 2007 French EAV outbreak was linked to an EAV strain present in the semen of a persistently infected carrier stallion.
Virology, 2011Co-Authors: Fabien Miszczak, Udeni B.r. Balasuriya, Aymeric Hans, Stéphane Pronost, Loïc Legrand, Guillaume Fortier, Jianqiang Zhang, Bénédicte Ferry-abitbol, Astrid VabretAbstract:Abstract During the summer of 2007, an outbreak of Equine Viral Arteritis (EVA) occurred in Normandy (France). After investigation, a link was suggested between an EAV carrier stallion (A) and the index premise of the outbreak. The full-length nucleotide sequence analysis of a study reference strain (F27) isolated from the lung of a foal revealed a 12,710 nucleotides EAV genome with unique molecular hallmarks in the 5′UTR leader sequence and the ORF1a sequence encoding the non-structural protein 2. The evolution of the Viral population in the persistently infected Stallion A was then studied by cloning ORFs 3 and 5 of the EAV genome from four sequential semen samples which were collected between 2000 and 2007. Molecular analysis of the clones confirmed the likely implication of Stallion A in the origin of this outbreak through the yearly emergence of new variants genetically similar to the F27 strain.
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evaluation of the safety of vaccinating mares against Equine Viral Arteritis during mid or late gestation or during the immediate postpartum period
Javma-journal of The American Veterinary Medical Association, 2011Co-Authors: C. C. Broaddus, Udeni B.r. Balasuriya, Peter J. Timoney, Jena White, Rebecca A Funk, Reed G HolyoakAbstract:Objective—To determine whether it is safe to vaccinate pregnant or postpartum mares with a commercial modified-live virus vaccine against Equine Viral Arteritis (EVA). Design—Randomized controlled study. Animals—73 mares and their foals. Procedures—Mares were vaccinated during mid gestation, during late gestation, or 2 or 3 days after parturition with a commercial modified-live virus vaccine or were not vaccinated. Foaling outcomes were recorded, and serum, blood, milk, and nasopharyngeal samples were obtained. Results—All mares vaccinated during mid gestation foaled without any problems; 21 of 22 mares in this group had antibody titers against EAV at the time of foaling. Of the 19 mares vaccinated during late gestation, 3 aborted; antibody titers against EAV were detected in 13 of 15 mares from which serum was obtained at the time of foaling. All postparturient vaccinates were seronegative at foaling; all of them seroconverted after vaccination. No adverse effects were detected in any of their foals. Con...
N. James Maclachlan - One of the best experts on this subject based on the ideXlab platform.
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Equine Arteritis virus.
Veterinary Microbiology, 2013Co-Authors: Udeni B.r. Balasuriya, N. James MaclachlanAbstract:Equine Arteritis virus (EAV) is the causative agent of Equine Viral Arteritis (EVA), a respiratory and reproductive disease of equids. There has been significant recent progress in understanding the molecular biology of EAV and the pathogenesis of its infection in horses. In particular, the use of contemporary genomic techniques, along with the development and reverse genetic manipulation of infectious cDNA clones of several strains of EAV, has generated significant novel information regarding the basic molecular biology of the virus. Therefore, the objective of this review is to summarize current understanding of EAV virion architecture, replication, evolution, molecular epidemiology and genetic variation, pathogenesis including the influence of host genetics on disease susceptibility, host immune response, and potential vaccination and treatment strategies.
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Equine Viral Arteritis
Advances in experimental medicine and biology, 2006Co-Authors: N. James Maclachlan, Udeni B.r. BalasuriyaAbstract:Equine Viral Arteritis (EVA) is an important if uncommon disease of horses. Potential economic losses attributable to EVA include direct losses from abortion, pneumonia in neonates, and febrile disease in performance horses. Indirect losses are those associated with national and international trade/animal movement regulations, particularly those pertaining to persistently infected carrier stallions and their semen. However, Equine Arteritis virus infection and EVA are readily prevented through serological and virological screening of horses, coupled with sound management practices that include appropriate quarantine and strategic vaccination.
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Growth characteristics of a highly virulent, a moderately virulent, and an avirulent strain of Equine Arteritis virus in primary Equine endothelial cells are predictive of their virulence to horses.
Virology, 2002Co-Authors: Brian D. Moore, Udeni B.r. Balasuriya, Jodi F. Hedges, N. James MaclachlanAbstract:Equine Viral Arteritis (EVA) is an endotheliotropic Viral disease of horses caused by Equine Arteritis virus (EAV). Although there is only one serotype of EAV, there is marked variation in the virulence of different strains of the virus. The replication and cytopathogenicity of three well-characterized strains of EAV of different virulence to horses were compared in rabbit kidney (RK-13) and primary Equine pulmonary artery endothelial cells (ECs). Viral protein expression, plaque size, and cytopathogenicity of all three viruses were similar in RK-13 cells, whereas two virulent strains of EAV were readily distinguished from an avirulent strain by their plaque morphology and cytopathogenicity in primary Equine ECs. Furthermore, EAV nucleocapsid protein was detected by flow cytometric analysis significantly later in ECs infected with the avirulent than those infected with the virulent strains of EAV. Primary Equine ECs provide a convenient and relevant model for in vitro characterization of the pathogenesis of EVA and the virulence determinants of EAV.
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Genetic stability of Equine Arteritis virus during horizontal and vertical transmission in an outbreak of Equine Viral Arteritis
Journal of General Virology, 1999Co-Authors: Udeni B.r. Balasuriya, Jodi F. Hedges, Peter J. Timoney, William H. Mccollum, Steven A. Nadler, N. James MaclachlanAbstract:An imported carrier stallion (A) from Europe was implicated in causing an extensive outbreak of Equine Viral Arteritis (EVA) on a Warmblood breeding farm in Pennsylvania, USA. Strains of Equine Arteritis virus (EAV) present in the semen of two carrier stallions (A and G) on the farm were compared to those in tissues of foals born during the outbreak, as well as viruses present in the semen of two other stallions that became persistently infected carriers of EAV following infection during the outbreak. The 2822 bp segment encompassing ORFs 2-7 (nt 9807-12628; which encode the G(S), GP3, GP4, G(L), M and N proteins, respectively) was directly amplified by RT-PCR from semen samples and foal tissues. Nucleotide and phylogenetic analyses confirmed that virus present in the semen of stallion A initiated the outbreak. The genomes of viruses present in most foal tissues (10/11) and serum from an acutely infected mare collected during the outbreak were identical to that of virus present in the lung of the first foal that died of EVA. Virus in the placenta of one foal differed by one nucleotide (99.9% identity) from the predominant outbreak virus. The relative genetic stability of viruses that circulated during the outbreak contrasts markedly with the heterogeneous virus populations variously present in the semen of persistently infected stallions on the farm. These findings are consistent with the hypothesis that the carrier stallion can be a source of genetic diversity of EAV, and that outbreaks of EVA can be initiated by the horizontal aerosol transmission of specific Viral variants that occur in the semen of particular carrier stallions.
Peter J. Timoney - One of the best experts on this subject based on the ideXlab platform.
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Equine Viral Arteritis a respiratory and reproductive disease of significant economic importance to the Equine industry
Equine Veterinary Education, 2018Co-Authors: U B R Balasuriya, Mariano Carossino, Peter J. TimoneyAbstract:Summary Equine Arteritis virus is the causative agent of Equine Viral Arteritis, a respiratory and reproductive disease that affects the members of the family Equidae. The virus was first isolated from the lung of an aborted fetus after an extensive outbreak of respiratory disease and abortion on a Standardbred breeding farm near Bucyrus, Ohio, in 1953. Since then, periodic outbreaks of Equine Viral Arteritis have been reported in a number of countries around the world. This disease may result in significant economic loss to the Equine industry due to the occurrence of abortion in pregnant mares, neonatal mortality, and establishment of the carrier state in stallions. This article provides an extensive review on Equine Arteritis virus, epidemiology, disease, pathogenesis, and prevention and control measures.
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evaluation of the safety of vaccinating mares against Equine Viral Arteritis during mid or late gestation or during the immediate postpartum period
Javma-journal of The American Veterinary Medical Association, 2011Co-Authors: C. C. Broaddus, Udeni B.r. Balasuriya, Peter J. Timoney, Jena White, Rebecca A Funk, Reed G HolyoakAbstract:Objective—To determine whether it is safe to vaccinate pregnant or postpartum mares with a commercial modified-live virus vaccine against Equine Viral Arteritis (EVA). Design—Randomized controlled study. Animals—73 mares and their foals. Procedures—Mares were vaccinated during mid gestation, during late gestation, or 2 or 3 days after parturition with a commercial modified-live virus vaccine or were not vaccinated. Foaling outcomes were recorded, and serum, blood, milk, and nasopharyngeal samples were obtained. Results—All mares vaccinated during mid gestation foaled without any problems; 21 of 22 mares in this group had antibody titers against EAV at the time of foaling. Of the 19 mares vaccinated during late gestation, 3 aborted; antibody titers against EAV were detected in 13 of 15 mares from which serum was obtained at the time of foaling. All postparturient vaccinates were seronegative at foaling; all of them seroconverted after vaccination. No adverse effects were detected in any of their foals. Con...
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Response of Stallions to Primary Immunization with a Modified Live Equine Viral Arteritis Vaccine
Journal of Equine Veterinary Science, 2011Co-Authors: K. Amy Summers-lawyer, Peter J. Timoney, Patrick M. Mccue, Jianqiang Zhang, Kathleen M. Shuck, Jason E. BruemmerAbstract:Abstract This study was undertaken to re-evaluate safety aspects of the commercial modified live virus vaccine against Equine Viral Arteritis (Arvac) in stallions. Ten seronegative stallions were administered a single dose of vaccine, whereas three others were used as controls. Presence of vaccine virus in blood, semen, and nasopharyngeal and conjunctival secretions was determined by virus isolation and reverse transcription-polymerase chain reaction assay. No adverse effects were observed after vaccination. Vaccine virus was detected in buffy-coat cultures of all stallions for an average of 4.3 days, and in nasopharyngeal swabs from 40% of the stallions for an average of 3.2 days. No virus was detected in conjunctival swabs. Small quantities of virus were detected in the semen of one stallion on days 4 and 6 postvaccination. Vaccinated stallions showed a marked increase in neutralizing antibody titers within 5 to 8 days after vaccination. The stallions in the control group remained uninfected. Finding very low levels of virus in the semen of one stallion provides justification for withholding semen from a first-time vaccinated stallion for a minimum of 14 days to avoid the potential risk of virus transmission or having vaccine virus detected in semen frozen from a recently vaccinated stallion. There was no evidence of persistence of vaccine virus in the reproductive tract of the vaccinated stallions. Virus isolation proved more sensitive than reverse transcription-polymerase chain reaction for detection of virus in buffy-coat and nasopharyngeal specimens. Peak antibody responses were reached at a little more than a week after vaccination and these remained undiminished for the remainder of the study.
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Equine Viral Arteritis: current status and prevention.
Theriogenology, 2008Co-Authors: G.r. Holyoak, Udeni B.r. Balasuriya, C. C. Broaddus, Peter J. TimoneyAbstract:Recently, there has been increased interest in Equine Viral Arteritis (EVA) among veterinarians and horse owners. Outbreaks of the disease were identified initially in New Mexico, USA in 2006, and in the Normandy region of France in the summer of 2007. Both occurrences were associated with AI of cool-shipped semen. Each was linked to respiratory illness, neonatal death, abortion, development of carrier stallions, and cancellation of equestrian events. In light of the increased interest, this paper will present a brief case history, followed by a review addressing common concerns regarding EVA, current status, and control and prevention strategies, including vaccination, and recommended bio-security measures.
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Equine Viral Arteritis: further characterization of the carrier state in stallions.
Journal of reproduction and fertility. Supplement, 2000Co-Authors: Peter J. Timoney, William H. MccollumAbstract:Further characterization of the carrier state in stallions infected with Equine Arteritis virus revealed that there is considerable variation in the frequency of its occurrence among breeds. The frequency ranged from 12.5% (Holsteiner stallions) to 72.7% (Dutch Warmblood stallions), with a mean occurrence of 40.8% in the seropositive stallions (n=561) examined. More than 70% of the virus shedders were Standardbred stallions. The carrier state was not confirmed in any of the stallions that had been vaccinated against Equine Viral Arteritis nor was there any evidence of intermittent virus shedding by carrier stallions. Most (98.2%) of the semen isolates of Equine Arteritis virus were obtained on first passage in RK-13 cell culture and most of the samples had very high virus infectivity titres. Intermediate term (3.5-7.0 months) and long-term (> or =1 year) carrier states were confirmed in various horse breeds. Long-term persistence of Equine Arteritis virus in individual stallions was common, and some animals continued to shed the virus in semen for 4-12 years. Spontaneous clearance of the carrier state was observed in 27 stallions after periods ranging from several months to many years. There was a considerable difference in the rate of clearance of the carrier state between Standardbred (4.3%) and Thoroughbred (42.3%) stallions. Reduction and eventual elimination of the carrier stallion reservoir of Equine Arteritis virus is the key to the success of any control programme for this disease.
Christine Ek-kommonen - One of the best experts on this subject based on the ideXlab platform.
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Equine Viral Arteritis
Advances in experimental medicine and biology, 1998Co-Authors: Anita Huovilainen, Christine Ek-kommonenAbstract:A serological study for antibodies against Equine Arteritis virus (EAV) in Finland was performed during 1996. All Equine sera delivered to the Virology Unit at the National Veterinary and Food Research Institute were tested with a micro-neutralization test, using the Arvac strain as antigen. The study also included imported horses to evaluate EAV circulation in the countries of origin.
Jodi F. Hedges - One of the best experts on this subject based on the ideXlab platform.
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Growth characteristics of a highly virulent, a moderately virulent, and an avirulent strain of Equine Arteritis virus in primary Equine endothelial cells are predictive of their virulence to horses.
Virology, 2002Co-Authors: Brian D. Moore, Udeni B.r. Balasuriya, Jodi F. Hedges, N. James MaclachlanAbstract:Equine Viral Arteritis (EVA) is an endotheliotropic Viral disease of horses caused by Equine Arteritis virus (EAV). Although there is only one serotype of EAV, there is marked variation in the virulence of different strains of the virus. The replication and cytopathogenicity of three well-characterized strains of EAV of different virulence to horses were compared in rabbit kidney (RK-13) and primary Equine pulmonary artery endothelial cells (ECs). Viral protein expression, plaque size, and cytopathogenicity of all three viruses were similar in RK-13 cells, whereas two virulent strains of EAV were readily distinguished from an avirulent strain by their plaque morphology and cytopathogenicity in primary Equine ECs. Furthermore, EAV nucleocapsid protein was detected by flow cytometric analysis significantly later in ECs infected with the avirulent than those infected with the virulent strains of EAV. Primary Equine ECs provide a convenient and relevant model for in vitro characterization of the pathogenesis of EVA and the virulence determinants of EAV.
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Alphavirus replicon particles expressing the two major envelope proteins of Equine Arteritis virus induce high level protection against challenge with virulent virus in vaccinated horses.
Vaccine, 2002Co-Authors: Udeni B.r. Balasuriya, Jodi F. Hedges, Nancy L Davis, Robert E Johnston, Hans W Heidner, Heike M Wagner, Pamela J Hullinger, Jacqueline C Williams, W David Wilson, Irwin K LiuAbstract:Replicon particles derived from a vaccine strain of Venezuelan Equine encephalitis (VEE) virus were used as vectors for expression in vivo of the major envelope proteins (G(L) and M) of Equine Arteritis virus (EAV), both individually and in heterodimer form (G(L)/M). The immunogenicity of the different replicons was evaluated in horses, as was their ability to protectively immunize horses against intranasal and intrauterine challenge with a virulent strain of EAV (EAV KY84). Horses immunized with replicons that express both the G(L) and M proteins in heterodimer form developed neutralizing antibodies to EAV, shed little or no virus, and developed only mild or inapparent signs of Equine Viral Arteritis (EVA) after challenge with EAV KY84. In contrast, unvaccinated horses and those immunized with replicons expressing individual EAV envelope proteins (M or G(L)) shed virus for 6-10 days in their nasal secretions and developed severe signs of EVA after challenge. These data confirm that replicons that co-express the G(L) and M envelope proteins effectively, induce EAV neutralizing antibodies and protective immunity in horses.
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Genetic stability of Equine Arteritis virus during horizontal and vertical transmission in an outbreak of Equine Viral Arteritis
Journal of General Virology, 1999Co-Authors: Udeni B.r. Balasuriya, Jodi F. Hedges, Peter J. Timoney, William H. Mccollum, Steven A. Nadler, N. James MaclachlanAbstract:An imported carrier stallion (A) from Europe was implicated in causing an extensive outbreak of Equine Viral Arteritis (EVA) on a Warmblood breeding farm in Pennsylvania, USA. Strains of Equine Arteritis virus (EAV) present in the semen of two carrier stallions (A and G) on the farm were compared to those in tissues of foals born during the outbreak, as well as viruses present in the semen of two other stallions that became persistently infected carriers of EAV following infection during the outbreak. The 2822 bp segment encompassing ORFs 2-7 (nt 9807-12628; which encode the G(S), GP3, GP4, G(L), M and N proteins, respectively) was directly amplified by RT-PCR from semen samples and foal tissues. Nucleotide and phylogenetic analyses confirmed that virus present in the semen of stallion A initiated the outbreak. The genomes of viruses present in most foal tissues (10/11) and serum from an acutely infected mare collected during the outbreak were identical to that of virus present in the lung of the first foal that died of EVA. Virus in the placenta of one foal differed by one nucleotide (99.9% identity) from the predominant outbreak virus. The relative genetic stability of viruses that circulated during the outbreak contrasts markedly with the heterogeneous virus populations variously present in the semen of persistently infected stallions on the farm. These findings are consistent with the hypothesis that the carrier stallion can be a source of genetic diversity of EAV, and that outbreaks of EVA can be initiated by the horizontal aerosol transmission of specific Viral variants that occur in the semen of particular carrier stallions.