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At least 127 records · Page 7Linked to original sources
PubMed1990

Induction of immune response and protection from equine viral arteritis (EVA) by formalin inactivated-virus vaccine for EVA in horses.

Thirty-nine horses included 3 pregnant mares were examined by inoculating with formalin inactivated-virus vaccine for EVA. Antibody response of horses after one dose vaccination was somewhat poor and 50% effective inoculum dose of the vaccine should be included 10(8.4) pfu of virus before inactivation. After 2 doses given at an interval of 4 weeks, the horses developed such high titer of SN antibody as up to 1:5,120. The SN titer declined rather rapidly, but supplemental administration of the vaccine at an interval of more than 2 months elicited a prompt antibody response and SN titers persisted as 1:80 to 1:320 at 6 months after the administration. Therefore, supplemental administration of the vaccine as booster every 6 months or 1 year would be capable of maintaining high titer of SN antibody. The inactivated-virus vaccine prevented horses from clinical disease of EVA and protected pregnant mares from abortion by challenge exposure with virulent virus. Fifty percent protective dose in SN titer of 1:43 was confirmed by clinical signs and viremia.

Animals↗
PubMed1995

Equine viral arteritis with abortions: serological and virological evidence in Germany.

An outbreak of clinical disease with abortions, suspected to be equine viral arteritis in Germany was examined serologically and virologically. Three of five animals tested seroconverted to EAV, and EAV was isolated from an aborted fetus. In view of the significant increase in seropositive horses, the need for control measures is emphasized.

Abortion, Veterinary↗
PubMed1996

Histopathological and immunofluorescent studies on transplacental infection in experimentally induced abortion by equine arteritis virus.

Five pregnant mares, at between 6 and 8 months gestation, were experimentally infected with the Bucyrus strain of equine arteritis virus (EAV). Of the five mares, four aborted and one died. The pathogenesis of the abortions was studied, using histopathologic techniques, tissue immunofluorescence and virus isolation. Common microscopic lesions in the maternal reproductive organs indicated myometritis with a degeneration of the myocytes and an infiltration of the mononuclear cells. Epithelial cells of the endometrial gland showed sporadic degeneration. Lesions in the fetal tissue included an atrophy of the lymphoid follicles in the spleen and lymph nodes with degenerated lymphocytes. The placentae were oedematous and degenerated fibroblasts were observed in the subvillous layers. Immunofluorescence detected EAV antigen in the myometrium and the endometrial gland in the dams, in the subvillous layer of the placentae, and in the aborted fetuses. EAV was recovered from the maternal uteri, placentae and fetuses. The placentae yielded the greatest amounts of the virus. Transplacental infection of the fetus was clearly demonstrated in the EAV infection.

Abortion, Veterinary↗
PubMed2005

A novel subgroup among genotypes of equine arteritis virus: genetic comparison of 40 strains.

The authors determined partial nucleic sequences of the variable regions of open-reading frame (ORF5) from 151 nucleotide to 668 nucleotide and deduced amino acid sequences of 518 nucleotide respectively of 20 equine arteritis virus (EAV) isolates. About 19 Hungarian and one Austrian EAV strains were subjected to sequence analysis, the further data of 20 EAV strains: six North American and 14 European were obtained from the GenBank. Comparative sequence analysis of the Hungarian EAV strains indicated that among the three variable regions the first has been affected mostly by point mutations. Genetic comparison of the Hungarian strains with other EAV isolates from western Europe and North America (including the Bucyrus reference strain) has been performed on the aforementioned genome region. Besides the already known genetic subgroups of EAV; phylogenetic analysis revealed a novel subgroup comprising mainly Hungarian strains. Compared with the Bucyrus virus, the overall sequence divergencies of the examined Hungarian strains ranged from 81.47 to 90.73% at nucleotide and from 84.88 to 91.86% at amino acid level. Epizootiological studies have shown that the significant part of the EAV strains having been existed in Hungary before and in 2000 belong to this unique cluster (II.D) which was not indicated in former phylogenetic studies. After 2000 new EAV strains emerged in Hungary, one of them causing abortions or neonatal death. The previously dominant 'Hungarian' EAV genotypes were replaced by these new strains belonging to North American and European subgroups (I.A, I.B, II.A, II.B). The anamnesis of these cases revealed connections with persistent virus shedder stallions, those were imported to the country after 2000 or have been infected abroad. One of these Hungarian stallions became the source of abortion storms in Hungarian studs.

Amino Acid Sequence↗
PubMed2006

Extended phylogeny of equine arteritis virus: division into new subgroups.

To determine a conclusive phylogeny, equine arteritis viruses from Italy, Austria, Hungary, Sweden, South Africa and other parts of the world were analysed by reverse-transcription polymerase chain reaction amplification and direct sequencing. The nucleotide sequences corresponding to the variable part of the large glycoprotein GP5, specified by open reading frame 5, were compared and added to a previously published phylogenetic tree in which a clear division between 'European' and 'American' type viruses had been established. Adding the sequences determined in this study and new sequences retrieved from GenBank revealed additional diversity and new subgroups.

Animals↗
PubMed1990

The occurrence of equine arteritis virus in Australia.

This paper reports the first isolation of equine arteritis virus (EAV) in Australia and serological evidence of exposure to EAV in Australian horses. Twelve Standardbred stallions imported from North America were found to shed EAV in semen. One hundred and seven stallions were tested for serum antibodies to EAV and 73% of Standardbred stallions tested were seropositive as compared to 8% of Thoroughbred stallions. Serum antibody was detected in 71% of Standardbred mares, 6% of Standardbred racehorses and 1% of Thoroughbred mares and racehorses. Examination of stored serums demonstrated that EAV had been present in Australia since at least 1975.

Animals↗
PubMed2001

Identification of equine herpesvirus 3 (equine coital exanthema virus), equine gammaherpesviruses 2 and 5, equine adenoviruses 1 and 2, equine arteritis virus and equine rhinitis A virus by polymerase chain reaction.

OBJECTIVE: To develop rapid (< 8 hour) tests using polymerase chain reaction (PCR) for the diagnosis of equine herpesvirus 3 (EHV3; equine coital exanthema virus), equine gammaherpesviruses 2 (EHV2) and EHV5, equine adenovirus 1 (EAdV1), EAdV2, equine arteritis virus (EAV), equine rhinitis A virus (ERAV; formerly equine rhinovirus 1) DESIGN: Either single round or second round (seminested) PCRs were developed and validated. METHODS: Oligonucleotide primers were designed that were specific for each virus, PCR conditions were defined and the specificity and sensitivity of the assays were determined. The application of the tests was validated using a number of independent virus isolates for most of the viruses studied. The PCRs were applied directly to clinical samples where samples were available. RESULTS: We developed a single round PCR for the diagnosis of EHV3, a seminested PCR for EHV2 and single round PCRs for EHV5, EAdV1, EAdV2 and RT-PCRs for EAV and ERAV. The PCR primer sets for each virus were designed and shown to be highly specific (did not amplify any recognised non-target template) and sensitive (detection of minimal amounts of virus) and, where multiple virus isolates were available all isolates were detected. CONCLUSION: The development and validation of a comprehensive panel of PCR diagnostic tests, predominantly for viruses causing equine respiratory disease, that can be completed within 8 hours from receipt of clinical samples, provides a major advance in the rapid diagnosis or exclusion diagnosis of these endemic equine virus diseases in Australia.

Adenoviridae↗
PubMed1995

Clinical features of the 1992 outbreak of equine viral arteritis in Spain.

During 1992, a widespread outbreak of Equine viral arteritis (EVA) occurred at a riding establishment near Barcelona, Spain. A total of 31 out of 186 horses on the premises displayed clinical signs, most frequently, fever, depression, mild ventral and limb oedema and a vesicular-erosive stomatitis, with hypersalivation, petechiations and small ulcerations. Affected horses developed illness of varying severity with only a few exhibiting a severe form of the disease and no mortality was recorded. Haematological and blood biochemical examination the most severely affected horses revealed a thrombocytopenia, slight leucocytosis with neutrophilia, lymphopenia and eosinopenia, an increase in plasma fibrinogen and a small rise in serum proteins and indirect bilirubin values. Diagnosis was confirmed by demonstration of seroconversion to equine arteritis virus in acute and convalescent phase sera. Attempted isolation of the virus from citrated blood samples proved unsuccessful.

Acute Disease↗
PubMed1997

A survey for antibodies to equine arteritis virus in donkeys, mules and zebra using virus neutralisation (VN) and enzyme linked immunosorbent assay (ELISA).

A seroepidemiological survey of donkeys in South Africa (n = 4300) indicated a wide distribution and increasing prevalence of antibodies to equine arteritis virus (EAV). Donkey sera inhibited equine arteritis virus infection in virus neutralisation (VN) tests and in ELISA specifically bound to a recombinant antigen derived from the Bucyrus isolate of EAV. These results suggest that donkeys have been exposed to the same serotype of this virus as circulates among horses. A good correlation existed between EAV neutralising antibody titres and ELISA absorbance values (0.8631); the ELISA was sensitive and specific (99.2% and 80.3% respectively) for donkey sera when compared to the VN test and the recombinant ELISA antigen did not cross-react with sera positive for common African equine pathogens. VN+ ELISA+ donkeys were also found in Morocco and Zimbabwe and seropositive mules in both South Africa and Morocco. No seropositive zebra (n = 266) were detected from game reserves or zoos in 9 countries. The results confirm that in addition to horses and donkeys, mules are naturally infected with EAV.

Animals↗
PubMed1997

Equine viral arteritis in newborn foals: clinical, pathological, serological, microbiological and immunohistochemical observations.

Clinical, pathological, immunohistochemical, serological and microbiological findings are described for 2 geographically and temporally distinct equine arteritis virus (EAV) epidemics in newborn foals. Outbreak A occurred at a commercial Standardbred breeding facility; Outbreak B began in a group of research animals. Clinical signs were severe and primarily referable to the respiratory tract. Fever and leucopenia and/or thrombocytopenia were observed in foals surviving for more than 24 h. The most common gross pathological findings were limited to the respiratory tract. Common histopathological findings included interstitial pneumonia, lymphocytic arteritis and periarteritis with fibrinoid necrosis of the tunica media. Renal tubular necrosis was noted in 2 foals. Immunoperoxidase histochemistry combined with virus isolation was diagnostic in all cases.

Animals↗
PubMed1997

Expression cloning and humoral immune response to the nucleocapsid and membrane proteins of equine arteritis virus.

To provide a convenient and sensitive method for the detection of equine arteritis virus (EAV)-specific serum antibodies, we developed an immunoblot assay employing the EAV nucleocapsid (N) and membrane (M) proteins expressed in a procaryotic expression vector (pMAL-c2) for the production of recombinant maltose-binding (MBP) fusion proteins (MBP-N and MBP-M). The antigenic reactivity of the recombinant fusion proteins and their Xa factor cleavage EAV products was confirmed by immunoblot using horse antisera to EAV. Some horse sera, however, showed immune reactivity to the MBP fusion partner protein. Based on a total of 32 horse sera analyzed for the presence of EAV antibodies by immunoblot, using the MBP-N or -M fusion proteins and the Xa factor cleavage EAV products, and in the serum neutralization test, there was 100% concordance between the assays. Sera from horses experimentally infected with EAV were reactive in the immunoblot test with both the MBP-N and the MBP-M fusion proteins by day 14 after EAV exposure. The reactivity continued to the end of the experiment at day 145 after infection. This immune reactivity correlated with the detection of neutralizing antibodies in the serum samples. Based on these findings, the recombinant N and M proteins might be useful for serodetection of EAV-infected animals.

ATP-Binding Cassette Transporters↗
PubMed2002

Importance of M-protein C terminus as substrate antigen for serodetection of equine arteritis virus infection.

Equine arteritis virus (EAV), an enveloped positive-stranded RNA virus, is the prototype of the arterivirus group. In a previous paper (A. Kheyar, S. Martin, G. St.-Laurent, P. J. Timoney, W. H. McCollum, and D. Archambault, Clin. Diagn. Lab. Immunol. 4:648-652, 1997), we have shown that the unglycosylated membrane (M) protein, which is composed of 162 amino acids (aa), is a major target of equine antibody to EAV. In order to determine the antigenic regions of the M protein, the cDNA encoding the M protein of EAV was inserted into the procaryotic expression vector pGEX-4T-1 to produce recombinant glutathione S-transferase-M fusion protein. Various deletion mutant clones, which covered the entire sequence of the M protein, were then generated by inverse PCR and expressed in Escherichia coli to examine, by a Western blot assay, the antigenic reactivity of the clone-derived truncated M proteins with sera from horses either experimentally or naturally infected with EAV. Deletion of the hydrophobic N-terminal 87 aa did not abolish immune reactivity of the protein with serum antibodies to EAV, thereby demonstrating the antigenicity of the C-terminal region (aa 88 to 162) of the M protein. Further truncations of the M-protein C-terminal domain defined particular linear epitope-containing amino acid sequence regions. However, only the M-protein C-terminal region was readily recognized by all EAV-specific horse antisera tested in this study. Based on these findings, only the M-protein C-terminal polypeptide composed of aa 88 to 162 is necessary to identify horse serum antibodies specific to the EAV M protein. Thus, this polypeptide might be useful for serodetection of EAV-infected animals.

Animals↗
PubMed1976

Hemagglutination by equine infectious anemia virus.

Equine infectious anemia (EIA) virus which was propagated on an equine dermal cell line agglutinated guinea pig erythrocytes. Viral fluids containing about 10(7.5) mean tissue culture infective doses/ml showed hemagglutinating (HA) titers ranging from 16 to 32 units/0.05 ml. Results of cesium chloride equilibrium density gradient centrifugation revealed that the hemagglutinin was inseparable from the virus particles. The hemagglutination reaction persisted over a wide range of temperature and pH, and the absence of divalent cations did not decrease its activity. The HA activity was stable at 4 degrees C but not at 56 degreesC. The activity was destroyed by virus-disrupting lipid solvents and moderately sensitive to a proteolytic enzyme. Neuraminidase enhanced HA activity slightly. Phospholipase C had no effect on HA titer, although it completely inactivated infectivity. It was relatively stable to ultraviolet irradiation. Thus, the hemagglutinin appears to be closely associated with virus particles, and its activity is dependent on the presence of its lipids and proteins. Hemagglutination was inhibited by sera from horses infected with EIA virus. Hemagglutinin receptors on the erythrocytes were inactivated by a proteolytic enzyme and formaldehyde but were not influenced by neuraminidase, sodium deoxycholate, or KIO4.

Animals↗