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Nikolaus Osterrieder - One of the best experts on this subject based on the ideXlab platform.
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Vaccination of foals with a modified live, Equid Herpesvirus-1 gM deletion mutant (RacHΔgM) confers partial protection against infection
Vaccine, 2019Co-Authors: Julia H. Kydd, Duncan Hannant, Robert S Robinson, Neil Bryant, Nikolaus OsterriederAbstract:Equid Herpesvirus-1 (EHV-1) causes respiratory and neurological disease and late gestation abortion in pregnant mares. Current vaccines contain either inactivated or live EHV-1, but fail to provide complete clinical or virological protection, namely prevention of nasopharyngeal shedding and cell-associated viraemia. Thus, the development of novel products, such as modified live virus (MLV) vaccines which stimulate virus-specific, humoral and cell mediated immune responses more effectively remains a priority. Two groups of weaned foals (n = 6 each group) were used in a longitudinal, prospective, experimental study to evaluate immune responses elicited by two vaccinations with a glycoprotein M (gM) deletion mutant of EHV-1 (RacHdeltagM). Following two concurrent intranasal and intramuscular inoculations six weeks apart, vaccinated (8.4 ± 0.2 months old) and control foals (6.2 ± 0.4 months) were challenge infected intranasally with EHV-1 Ab4/8 four weeks after the second vaccination and clinical signs and virological replication measured. Vaccination caused no adverse events, but did stimulate significantly higher complement fixing and virus neutralizing antibodies in serum compared with control foals at either equivalent or pre-vaccination time points. Virus-specific nasopharyngeal antibody levels and cytotoxic T lymphocyte responses were not significantly different between the groups. Following challenge infection, these immune responses were associated with a reduction in clinical signs and virological replication in the vaccinated foals, including a reduction in duration and magnitude of pyrexia, nasopharyngeal shedding and cell-associated viraemia. We conclude that the RacHΔgM MLV primed EHV-1-specific humoral immune responses in weaned foals. However, complete virological protection by vaccination against EHV-1 requires further research.
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Equid Herpesvirus 1 (EHV1) infection of equine mesenchymal stem cells induces a pUL56-dependent downregulation of select cell surface markers.
Veterinary microbiology, 2014Co-Authors: Christophe Claessen, Nikolaus Osterrieder, Herman Favoreel, Catharina De Schauwer, Sofie Piepers, Gerlinde R Van De WalleAbstract:Equid Herpesvirus 1 (EHV1) is an ubiquitous alphaHerpesvirus that can cause respiratory disease, abortion and central nervous disorders. EHV1 is known to infect a variety of different cell types in vitro, but its tropism for cultured primary equine mesenchymal stem cells (MSC) has never been explored. We report that equine MSC were highly permissive for EHV1 and supported lytic replication of the virus in vitro. Interestingly, we observed that an infection of MSC with EHV1 resulted in a consistent downregulation of cell surface molecules CD29 (β1-integrin), CD105 (endoglin), major histocompatibility complex type I (MHCI) and a variable downregulation of CD172a. In contrast, expression of CD44 and CD90 remained unchanged upon wild type infection. In addition, we found that this selective EHV1-mediated downregulation of cell surface proteins was dependent on the viral protein UL56 (pUL56). So far, pUL56-dependent downregulation during EHV1 infection of equine cells has only been described for MHCI, but our present data indicate that pUL56 may have a broader function in downregulating cell surface proteins. Taken together, our results are the first to show that equine MSC are susceptible for EHV1 and that pUL56 induces downregulation of several cell surface molecules on infected cells. These findings provide a basis for future studies to evaluate the mechanisms underlying for this selective pUL56-induced downregulation and to evaluate the potential role of MSC during EHV1 pathogenesis.
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Venereal shedding of Equid Herpesvirus-1 (EHV-1) in naturally infected stallions.
Journal of veterinary internal medicine, 2012Co-Authors: Jasmin Walter, Hans-jörg Balzer, Christoph Seeh, Kerstin Fey, Ulrich Bleul, Nikolaus OsterriederAbstract:Background Equid Herpesvirus 1 (EHV-1) is a highly prevalent pathogen in horse populations worldwide. Oronasal infection represents the classic route of disease transmission. Venereal shedding of EHV-1 is not regarded relevant in terms of virus spreading, which is in contrast to the close relatives of EHV-1, bovine and suid alphaHerpesvirus, for which artificial insemination is a well-documented and accepted means of virus spread. Objectives Documentation of venereal EHV-1 shedding in 3 naturally infected stallions. Animals Three stallions were infected during an acute outbreak by an EHV-1 strain with the G2254/D752 Pol genotype. Methods In this observational study, 12 semen samples from these 3 stallions were tested for EHV-1 to determine venereal shedding. EHV-1 was diagnosed by conventional PCR and paired serum neutralization tests in 42 horses. Semen samples were separated into sperm and seminal plasma fractions and tested for EHV-1 by conventional and quantitative PCR as well as virus isolation by cell culture. Results Acute EHV-1 infection was diagnosed on the premise. Five semen samples collected from 2 of the 3 stallions tested positive for EHV-1 by (q)PCR. On days 18 and 20 after onset of fever, the last positive samples were retrieved. All samples were positive in seminal plasma, only three in sperm fraction. Virus isolation attempts were unsuccessful. Conclusions and Clinical Importance The data presented here document shedding of EHV-1 in semen of naturally infected stallions for close to 3 weeks, which seems not to be directly associated with spermatozoa.
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Herpesviruses - a zoonotic threat?
Veterinary Microbiology, 2010Co-Authors: B. Karsten Tischer, Nikolaus OsterriederAbstract:Herpesviruses are highly host specific and share a long synchronous evolution with their hosts. Only in rare cases, species barriers fall and allow animal to human or human to animal transmission. Among the zoonotic Herpesviruses, is the most significant and can be transmitted from macaques to human. Conversely, is capable of causing severe disease in primates. Besides those two examples, there are several Herpesviruses with a certainly limited or only suspected ability to cross species barriers. Those include , , Equid Herpesvirus 1, Epstein-Barr Virus, Marek's disease virus, and pseudorabies virus. Concerning xenotransplantations, porcine gammaHerpesviruses must be considered as a zoonotic threat.
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Herpesviruses - a zoonotic threat?
Veterinary Microbiology, 2010Co-Authors: B. Karsten Tischer, Nikolaus OsterriederAbstract:Herpesviruses are highly host specific and share a long synchronous evolution with their hosts. Only in rare cases, species barriers fall and allow animal to human or human to animal transmission. Among the zoonotic Herpesviruses, Cercopithecine Herpesvirus 1 is the most significant and can be transmitted from macaques to human. Conversely, Human Herpesvirus 1 is capable of causing severe disease in primates. Besides those two examples, there are several Herpesviruses with a certainly limited or only suspected ability to cross species barriers. Those include Saimiriine Herpesvirus 2, Phocid Herpesvirus 2, Equid Herpesvirus 1, Epstein-Barr Virus, Marek's disease virus, and Pseudorabies virus. Concerning xenotransplantations, porcine gammaHerpesviruses must be considered as a zoonotic threat.
N. Edington - One of the best experts on this subject based on the ideXlab platform.
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gonadotrophin
2013Co-Authors: D. J. Smith, A Purewal, A.s. Hamblin, J Iqbal, N. EdingtonAbstract:In vitro reactivation of latent Equid Herpesvirus-1 fro
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Equid Herpesvirus 1 infection of endothelial cells requires activation of putative adhesion molecules: an in vitro model.
Clinical and experimental immunology, 2002Co-Authors: D. J. Smith, A.s. Hamblin, N. EdingtonAbstract:SUMMARY Antisera to activated equine endothelial cells, which detected surface molecules of 116 kD, 97 kD, 42 kD and 38 kD, were made to investigate the role of endothelial adhesion molecules in Equid herpes virus 1 infection. These putative adhesion molecules could be induced by 17-β oestradiol, chorionic gonadotrophin, or IL-2, as well as by LPS and PWM. In an in vitro flow system, using equine veins or arteries, Equid Herpesvirus 1 in leucocytes was only transferred to infect endothelial cells if both leucocytes and endothelial cells expressed these surface molecules. Blocking of the membrane molecules with polyclonal antibodies prevented transfer of virus to the endothelial cells, indicating that the adhesion molecules had a key role in effecting transfer of virus. These in vitro observations give particular insight into the reports that in the natural course of infection in horses infection of endothelial cells is restricted to certain tissues, and in a wider context the results illustrate the complexity of factors that may direct tissue tropism.
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Equid Herpesvirus 1: platelets and alveolar macrophages are potential sources of activated TGF-B1 in the horse
Veterinary Immunology and Immunopathology, 2000Co-Authors: P M Chesters, A Hughes, N. EdingtonAbstract:Cell mediated responses to Equid Herpesvirus 1 (EHV-1) are of short duration in vivo and require considerable expansion to be detected in vitro. Raised serum levels of active transforming growth factor B (TGF-B1) have been shown to depress proliferative T cell responses in experimental infections with EHV-1 in ponies. The present work indicates that latent transforming growth factor B (TGF-B1) is present in circulating platelets, lymph node, bronchial epithelium and alveolar macrophages. Activation of platelets in vitro by thrombin resulted in the release of latent TGF-B1 from platelets, with a pg level of conversion to active TGF-B1, but virus alone did not activate TGF-B1. Exposure of circulating leucocytes to EHV-1 in vivo or in vitro does not result in detection of active TGF-B1 above residual levels that could be attributed to activation of platelets by manipulation. However, alveolar macrophages obtained by lavage at autopsy yield both latent and active TGF-B1 in ng quantities. Bronchial epithelium, and mesenteric lymph node leucocytes had equivalent levels of latent TGF-B1, but horses varied as to whether these tissues were a source of activated TGF-B1 and as to whether EHV-1 activated TGF-B1.
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In vitro reactivation of latent Equid Herpesvirus-1 from CD5+/CD8+ leukocytes indirectly by IL-2 or chorionic gonadotrophin.
Journal of General Virology, 1998Co-Authors: D. J. Smith, A.s. Hamblin, Amarjit S Purewal, J Iqbal, N. EdingtonAbstract:IL-2 and equine chorionic gonadotrophin (eCG) initiated reactivation of Equid Herpesvirus-1 (EHV-1) from venous lymphocytes at a frequency of 1/10(-5). Indirect immunofluorescence showed that > 80% of virus-positive leukocytes were CD5+/CD8+ with the remaining 20% being CD5+/CD8-/CD4-. Cocultivation demonstrated that the reactivated virus was infectious. In addition, virus was reactivated in vitro from leukocytes of > 70% of horses by the mitogens phytohaemagglutinin (PHA) and pokeweed mitogen (PWM). Transfer of supernatants showed that IL-2 and eCG acted indirectly by causing the release of other mediators from adherent cells; these mediators then reactivated EHV-1 from T cells. Blocking experiments with anti-IL-2 showed that PWM and PHA acted via IL-2 but that eCG did not. This is the first clear definition of the lymphoid cells that harbour latent EHV-1 in vivo and correlates with current RT-PCR and in situ hybridization of latency-associated transcripts in lymphocytes. This method of reactivation in vitro can be used to detect horses carrying latent EHV-1 in vivo and also has the potential to dissect the sequence of events involved in reactivation in vitro.
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in vitro reactivation of latent Equid Herpesvirus 1 from cd5 cd8 leukocytes indirectly by il 2 or chorionic gonadotrophin
Journal of General Virology, 1998Co-Authors: D. J. Smith, A.s. Hamblin, Amarjit S Purewal, J Iqbal, N. EdingtonAbstract:IL-2 and equine chorionic gonadotrophin (eCG) initiated reactivation of Equid Herpesvirus-1 (EHV-1) from venous lymphocytes at a frequency of 1/10(-5). Indirect immunofluorescence showed that > 80% of virus-positive leukocytes were CD5+/CD8+ with the remaining 20% being CD5+/CD8-/CD4-. Cocultivation demonstrated that the reactivated virus was infectious. In addition, virus was reactivated in vitro from leukocytes of > 70% of horses by the mitogens phytohaemagglutinin (PHA) and pokeweed mitogen (PWM). Transfer of supernatants showed that IL-2 and eCG acted indirectly by causing the release of other mediators from adherent cells; these mediators then reactivated EHV-1 from T cells. Blocking experiments with anti-IL-2 showed that PWM and PHA acted via IL-2 but that eCG did not. This is the first clear definition of the lymphoid cells that harbour latent EHV-1 in vivo and correlates with current RT-PCR and in situ hybridization of latency-associated transcripts in lymphocytes. This method of reactivation in vitro can be used to detect horses carrying latent EHV-1 in vivo and also has the potential to dissect the sequence of events involved in reactivation in vitro.
Duncan Hannant - One of the best experts on this subject based on the ideXlab platform.
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Vaccination of foals with a modified live, Equid Herpesvirus-1 gM deletion mutant (RacHΔgM) confers partial protection against infection
Vaccine, 2019Co-Authors: Julia H. Kydd, Duncan Hannant, Robert S Robinson, Neil Bryant, Nikolaus OsterriederAbstract:Equid Herpesvirus-1 (EHV-1) causes respiratory and neurological disease and late gestation abortion in pregnant mares. Current vaccines contain either inactivated or live EHV-1, but fail to provide complete clinical or virological protection, namely prevention of nasopharyngeal shedding and cell-associated viraemia. Thus, the development of novel products, such as modified live virus (MLV) vaccines which stimulate virus-specific, humoral and cell mediated immune responses more effectively remains a priority. Two groups of weaned foals (n = 6 each group) were used in a longitudinal, prospective, experimental study to evaluate immune responses elicited by two vaccinations with a glycoprotein M (gM) deletion mutant of EHV-1 (RacHdeltagM). Following two concurrent intranasal and intramuscular inoculations six weeks apart, vaccinated (8.4 ± 0.2 months old) and control foals (6.2 ± 0.4 months) were challenge infected intranasally with EHV-1 Ab4/8 four weeks after the second vaccination and clinical signs and virological replication measured. Vaccination caused no adverse events, but did stimulate significantly higher complement fixing and virus neutralizing antibodies in serum compared with control foals at either equivalent or pre-vaccination time points. Virus-specific nasopharyngeal antibody levels and cytotoxic T lymphocyte responses were not significantly different between the groups. Following challenge infection, these immune responses were associated with a reduction in clinical signs and virological replication in the vaccinated foals, including a reduction in duration and magnitude of pyrexia, nasopharyngeal shedding and cell-associated viraemia. We conclude that the RacHΔgM MLV primed EHV-1-specific humoral immune responses in weaned foals. However, complete virological protection by vaccination against EHV-1 requires further research.
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Evidence for non‐specific immunosuppression during the development of immune responses to Equid Herpesvirus‐1
Equine Veterinary Journal, 2010Co-Authors: Duncan Hannant, D. M. Jessett, T. O'neill, Jennifer A. MumfordAbstract:Summary Six ponies were experimentally infected with an isolate of Equid Herpesvirus type 1 (EHV-I) recovered from an aborted foetus. Clinical, virological and serological observations confirmed that infection was established in all ponies. EHV-I specific cellular immune responses as measured by T cell proliferation developed in parallel with specific antibody. In contrast to this, non-specific lymphocyte function was shown to be compromised after infection in that polyclonal T cell activation was depressed for at least 40 days. The dissociation of specific and non-specific cellular immune responses suggests that an immunological defect may develop in horses after EHV-I infection. The mechanism for this immunosuppression is not understood but it is unlikely to reflect a reduction in responding lymphocyte numbers in vivo because the observed immunosuppression continued well beyond the period of transient leucopaenia commonly seen with EHV-1.
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Virulence of the V592 isolate of Equid Herpesvirus-1 in ponies.
Journal of comparative pathology, 2000Co-Authors: Ken C. Smith, J. A. Mumford, Duncan Hannant, Katherine E. Whitwell, A. S. Blunden, J. P. TearleAbstract:The V592 strain of Equid Herpesvirus-1 (EHV-1), which was originally isolated from a fetus during an abortion epizootic, has proved to be of low virulence in infection studies. Five Welsh Mountain pony mares and one foal were challenged intranasally or by aerosol with this isolate, and monitored clinically and virologically. All six animals shed virus in nasopharyngeal mucus, and viraemia was recorded from day 7 post-infection (PI). Pathological investigations revealed mild rhinitis and bronchiolitis in the mares, with viral antigen expression in degenerating epithelial cells of the nasal mucosa and bronchioles, and in occasional monocytes in the respiratory tract-associated lymph nodes. Viral antigen expression was not detected in vascular endothelium of the mares, although vasculitis was seen to have affected small numbers of blood vessels in the dorsocaudal lung regions of a mare examined on day 10 PI. In the foal, respiratory lesions of a more localized nature included infection of vascular endothelium and associated vasculitis. The foal also had localized encephalitis affecting the olfactory lobes of the brain, with viral antigen expression in degenerating olfactory neurons and microglia. The data suggest that the relatively low virulence of strain V592 is associated with a lower degree of endotheliotropism than that shown by the highly virulent Ab4 and Army 183 isolates, and that this property is influenced by host immunity.
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Equid Herpesvirus-Induced Associated with Lymphoid Circulating Immunosuppression is Cells and Not Soluble Factors
Viral immunology, 1999Co-Authors: Duncan Hannant, T. O'neill, J H Kydd, E.n. Ostlund, P.j. Hopkin, J. A. MumfordAbstract:ABSTRACT A paresis isolate of Equid Herpesvirus 1 (EHV1, Ab4/8) and a plaque-purified virus derived from it (EHV1, Ab4/13), induced long-term suppression of both mitogenic and antigen-specific lymphocyte proliferations in adult outbred ponies. Peripheral blood mononuclear cells (PBMC) taken from a pony after EHV1 infection suppressed the in vitro function of normal cells but serum did not. This showed that the observed immune suppression was associated with circulating PBMC and/or their products rather than circulating soluble factors such as antigen or immune complexes. The results suggested that productive infection of lymphocytes by EHV1 was unlikely to result in the observed in vitro effects. Moreover, prostaglandin release from monocytes was not likely to have caused the observed suppression, because lymphocyte responsiveness was not restored in the presence of indomethacin.
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Residence and recruitment of leucocytes to the equine lung after EHV-1 infection.
Veterinary immunology and immunopathology, 1996Co-Authors: Julia H. Kydd, Duncan Hannant, J. A. MumfordAbstract:Abstract This study characterised bronchoalveolar leucocytes collected by lavage from five susceptible and two immune ponies before and after nebulised aerosol infection with Equid Herpesvirus-1 (EHV-1). Leucocyte counts and lymphocyte phenotypic analyses were performed using either differential staining or an indirect immunofluorescence assay with monoclonal antibodies specific for equine (Eq) CD4, CD5, CD8 and B lymphocytes. After EHV-1 infection, significant changes developed: a transient neutrophilia occurred on Day 2, coincident with a reduction in macrophage numbers and an EqCD5 + , EqCD4 + and EqCD8 + lymphopaenia. On Day 21, a significant rise in EqCD8 + lymphocytes with an associated fall in the EqCD4 + : EqCD8 + ratio and fluctuations in B lymphocyte phenotypes were observed. This study shows that following EHV-1 infection, the bronchoalveolar compartment is subject to dynamic leucocyte migration which may have an important role in immunopathogenesis and recovery from disease.
Jennifer A. Mumford - One of the best experts on this subject based on the ideXlab platform.
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Evidence for non‐specific immunosuppression during the development of immune responses to Equid Herpesvirus‐1
Equine Veterinary Journal, 2010Co-Authors: Duncan Hannant, D. M. Jessett, T. O'neill, Jennifer A. MumfordAbstract:Summary Six ponies were experimentally infected with an isolate of Equid Herpesvirus type 1 (EHV-I) recovered from an aborted foetus. Clinical, virological and serological observations confirmed that infection was established in all ponies. EHV-I specific cellular immune responses as measured by T cell proliferation developed in parallel with specific antibody. In contrast to this, non-specific lymphocyte function was shown to be compromised after infection in that polyclonal T cell activation was depressed for at least 40 days. The dissociation of specific and non-specific cellular immune responses suggests that an immunological defect may develop in horses after EHV-I infection. The mechanism for this immunosuppression is not understood but it is unlikely to reflect a reduction in responding lymphocyte numbers in vivo because the observed immunosuppression continued well beyond the period of transient leucopaenia commonly seen with EHV-1.
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evidence for non specific immunosuppression during the development of immune responses to Equid Herpesvirus 1
Equine Veterinary Journal, 2010Co-Authors: D Hannant, D. M. Jessett, T Oneill, Jennifer A. MumfordAbstract:Summary Six ponies were experimentally infected with an isolate of Equid Herpesvirus type 1 (EHV-I) recovered from an aborted foetus. Clinical, virological and serological observations confirmed that infection was established in all ponies. EHV-I specific cellular immune responses as measured by T cell proliferation developed in parallel with specific antibody. In contrast to this, non-specific lymphocyte function was shown to be compromised after infection in that polyclonal T cell activation was depressed for at least 40 days. The dissociation of specific and non-specific cellular immune responses suggests that an immunological defect may develop in horses after EHV-I infection. The mechanism for this immunosuppression is not understood but it is unlikely to reflect a reduction in responding lymphocyte numbers in vivo because the observed immunosuppression continued well beyond the period of transient leucopaenia commonly seen with EHV-1.
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Distribution of Equid Herpesvirus-1 (EHV-1) in the respiratory tract of ponies: implications for vaccination strategies.
Equine veterinary journal, 1994Co-Authors: Julia H. Kydd, Georgia J. Livesay, Ken C. Smith, Duncan Hannant, Jennifer A. MumfordAbstract:Summary Twelve adult ponies and 2 conventional foals were exposed to 106.6 TCID50 of Equid Herpesvirus-1 (EHV-1), strain Ab4 and samples of respiratory tract tissues were recovered. Infectious virus in tissue homogenates was detected using susceptible cell monolayers and expression of viral antigens was monitored using indirect immunoperoxidase histochemistry of paraffin sections. The results illustrated the rapid dissemination of EHV-1 throughout the respiratory tract, with early replication in the lungs one day after exposure. Endothelial cell infection was prominent in all areas of the nasopharynx by Day 4 emphasising the role of endotheliotropism and viraemia in dissemination of this virus to sites of secondary replication. Clinical disease in the adult ponies was mild.
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Distribution of Equid Herpesvirus-1 (EHV-1) in respiratory tract associated lymphoid tissue: implications for cellular immunity.
Equine veterinary journal, 1994Co-Authors: Julia H. Kydd, Georgia J. Livesay, Ken C. Smith, Duncan Hannant, Jennifer A. MumfordAbstract:Summary Twelve adult ponies and 2 conventional foals were exposed intranasal to EHV-1, strain Ab4 (TCID50 10−6.6) and samples of respiratory tract associated lymphoid tissues were recovered between 12 h and 13 days after infection. Infectious virus was detected in tissue homogenates using susceptible cell monolayers and expression of viral antigens was monitored using indirect immunoperoxidase histochemistry on paraffin sections. The results showed both infectious EHV-1 and viral antigens in respiratory tract associated lymph nodes 12 h after exposure. Infected leucocytes were identified morphologically as lymphocytes, monocytes, macrophages and plasma cells. The rapid intracellular localisation of EHV-1 in lymph nodes implies that cell mediated immunity is an important aspect of the equine response to this virus.
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An immunohistological study of the uterus of mares following experimental infection by Equid Herpesvirus 1
Equine veterinary journal, 1993Co-Authors: Ken C. Smith, S.m. Gower, Duncan Hannant, Jennifer A. Mumford, Katherine E. Whitwell, J. P. TearleAbstract:Summary Twelve Welsh Mountain pony mares in late gestation were infected intranasally with EHV-1 (AB4 isolate) at dose rates from 103 to 107.3 TCID50. This resulted in 3 cases of paresis, at Days 9, 10 and 12 after inoculation, and 5 abortions, at Days 6, 9, 18, 19 and 20. Euthanasia was performed between Days 6 and 21, with collection of uterine specimens for histopathology, virus isolation and immunoperoxidase staining from the pregnant horn, non-pregnant horn and body. EHV-1 replication in endometrial vessels was detected as early as Day 6 and was maximal at Days 9–11, when widespread thromboischaemic damage was present. By Days 15–19 in mares remaining pregnant, EHV-1 antigen expression in the endometrium was sparse, despite residual lesions but little associated thrombosis. Endometrial vascular pathology varied considerably in degree and extent, and no consistent predilection sites for replication within the uterus were apparent.
Ken C. Smith - One of the best experts on this subject based on the ideXlab platform.
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Virulence of the V592 isolate of Equid Herpesvirus-1 in ponies.
Journal of comparative pathology, 2000Co-Authors: Ken C. Smith, J. A. Mumford, Duncan Hannant, Katherine E. Whitwell, A. S. Blunden, J. P. TearleAbstract:The V592 strain of Equid Herpesvirus-1 (EHV-1), which was originally isolated from a fetus during an abortion epizootic, has proved to be of low virulence in infection studies. Five Welsh Mountain pony mares and one foal were challenged intranasally or by aerosol with this isolate, and monitored clinically and virologically. All six animals shed virus in nasopharyngeal mucus, and viraemia was recorded from day 7 post-infection (PI). Pathological investigations revealed mild rhinitis and bronchiolitis in the mares, with viral antigen expression in degenerating epithelial cells of the nasal mucosa and bronchioles, and in occasional monocytes in the respiratory tract-associated lymph nodes. Viral antigen expression was not detected in vascular endothelium of the mares, although vasculitis was seen to have affected small numbers of blood vessels in the dorsocaudal lung regions of a mare examined on day 10 PI. In the foal, respiratory lesions of a more localized nature included infection of vascular endothelium and associated vasculitis. The foal also had localized encephalitis affecting the olfactory lobes of the brain, with viral antigen expression in degenerating olfactory neurons and microglia. The data suggest that the relatively low virulence of strain V592 is associated with a lower degree of endotheliotropism than that shown by the highly virulent Ab4 and Army 183 isolates, and that this property is influenced by host immunity.
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Systemic infection by Equid Herpesvirus-1 in a Grevy's zebra stallion (Equus grevyi) with particular reference to genital pathology
Journal of comparative pathology, 1998Co-Authors: A. S. Blunden, Ken C. Smith, Katherine E. Whitwell, K. A. DunnAbstract:Summary A severe multi-systemic form of Equid Herpesvirus-1 infection is described in an adult zebra stallion. There was multifocal necrotizing rhinitis marked hydrothorax and pulmonary oedema, with viral antigen expression in degenerating epithelial cells, local endothelial cells and intravascular leucocytes of the nasal mucosa and lung. Specific localization of EHV-1 infection was seen in the testes and epididymides, including infection of Leydig cells and germinal epithelium, which would have facilitated venereal shedding of virus in life. The case provided a unique opportunity to study hitherto undescribed aspects of the pathogenesis of naturally occurring EHV-1 infection in the male equine genital tract. Restriction digests of the isolate demonstrated a pattern similar to that of EHV-1 isolates previously recovered from aborted zebra and onager fetuses.
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Herpesviral abortion in domestic animals
Veterinary journal (London England : 1997), 1997Co-Authors: Ken C. SmithAbstract:Summary Abortion or neonatal disease may follow infection with several α, β and γ-Herpesviruses. The α-Herpesvirus, Equid Herpesvirus-1 (EHV-1), causes single or epizootic abortions or neonatal deaths in Equids, and the closely related virus EHV-4 causes sporadic equine abortions. In cattle, the α-Herpesviruses, bovine Herpesvirus-1 (infectious bovine rhinotracheitis virus) and bovine Herpesvirus-5 (bovine encephalitis virus), and a γ-Herpesvirus, bovine Herpesvirus-4, have all been implicated as causes of abortion. In pigs, suid Herpesvirus-1 (SHV-1: pseudorabies virus), an α-Herpesvirus, and SHV-2 (porcine cytomegalovirus), a β-Herpesvirus, each cause abortion or neonatal piglet losses. Caprine Herpesvirus-1, canine Herpesvirus and feline Herpesvirus-1, all α-Herpesviruses, cause abortions or neonatal deaths in goats, dogs and cats, respectively. This review discusses the pathogenesis, pathology and laboratory diagnosis of these herpesviral abortions and neonatal diseases, with an emphasis on experimental studies of each disease. Alternative reviews covering other aspects of each infection, such as the genetic and antigenic structure of the viruses, host immune responses and approaches to vaccination and disease control are indicated at appropriate points in the text. nts in the text.
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Use of transabdominal ultrasound-guided amniocentesis for detection of Equid Herpesvirus 1-induced fetal infection in utero.
American journal of veterinary research, 1997Co-Authors: Ken C. Smith, Matthew M. BinnsAbstract:OBJECTIVE To evaluate transabdominal ultrasound-guided amniocentesis for detection of Equid herpes-virus 1 (EHV-1)-induced fetal infection in utero. ANIMALS 4 Welsh Mountain mares. PROCEDURE Pregnant mares were inoculated intranasally with EHV-1 during the ninth month of gestation. Amniocentesis was initiated on postinoculation day (PID) 12, and was performed at 2- to 3-day intervals in standing mares under deep sedation. Amniotic fluid samples were tested by virus isolation (VI), polymerase chain reaction (PCR), and immunoperoxidase cytologic examination (IC) for detection of EHV-1. RESULTS Exposure to EHV-1 in the ninth month of gestation resulted in nasal shedding of infective virus, establishment of cell-associated viremia, and seroconversion. Equid Herpesvirus 1 was detected by VI, PCR, and IC in amniotic fluid collected on PID 14 from 1 mare and on PID 16 and 17 from a second mare. Specimens of amniotic fluid from a third mare were VI negative until PID 18, when collections ceased, although this mare subsequently aborted an EHV-1-infected fetus on PID 28. The fourth mare aborted an EHV-1 infected fetus on PID 14. The 2 mares with VI-positive amniotic fluid were each carrying an EHV-1 infected fetus in utero, confirmed by examination of the uterus, placenta, and fetus, using specific immunohistochemistry and in situ hybridization. Endothelial cells in the endometrium and allantochorion were often virus-infected, with accompanying vascular lesions. The fetus had been infected via the chorionic vasculature in the first and fourth mares, and by inhalation of infected amniotic fluid in the second mare. CONCLUSION Amniocentesis permits specific detection of EHV-1-induced fetal infection in utero. CLINICAL RELEVANCE Amniocentesis may have a clinical role in the specific identification and isolation of mares carrying virus-infected fetuses during EHV-1-induced abortion epizootics.
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Replication of Equid Herpesvirus-1 (EHV-1) in the testes and epididymides of ponies and venereal shedding of infectious virus.
Journal of Comparative Pathology, 1996Co-Authors: J. P. Tearle, M.s. Boyle, Georgia J. Livesay, Ken C. Smith, Matthew M. Binns, Jeanette A MumfordAbstract:Summary Six Welsh Mountain pony colts were infected intranasally with the Ab4 isolate of EHV-1. Clinical and virological monitoring demonstrated mild upper respiratory tract disease, with nasal shedding of virus and establishment of a cell-associated viraemia. Detailed pathological examination of the urogenital tract was performed post mortem on days 4–9 post-infection (PI). EHV-1 was isolated from the epididymis on day 8 and the testis on day 9 PI, with viral replication in endothelial cells of these organs and an associated necrotizing vasculitis and thrombosis. Productive viral infection of germinal epithelium was not observed. In a further study, three Welsh Mountain pony stallions were infected intranasally with Ab4, which again resulted in mild upper respiratory tract disease and the establishment of a cell-associated viraemia. Semen samples were collected up to day 60 PI. Two stallions showed a decrease in the proportion of morphologically normal sperm. Significant numbers of inflammatory cells were observed in the sperm-rich fraction of ejaculates collected from one stallion between days 16 and 28 PI; infectious virus was recovered from the semen of this animal between days 17 and 25 PI, after the cessation of viraemia. The affected stallion appeared clinically normal over the period of venereal EHV-1 shedding.