Rapid subtyping of equine herpesvirus 1 with monoclonal antibodies

Yeargan, Michelle R.; Allen, George P.; Bryans, J T

doi:10.1128/jcm.21.5.694-697.1985

Cited by 53 publications

(15 citation statements)

References 8 publications

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“…Clinical signs of EHV-1 infection in young horses consist of fever, serous to mucopurulent nasal discharge, occasional coughing and local lymphomegaly (Doll et al 1954;Bryans 1964Bryans , 1980Coggins 1979), whereas infections in older horses are often mild or subclinical (Bryans 1980(Bryans , 1981. EHV-I infection cannot be distinguished from EHV-4 infection clinically in the field but monoclonal antibodies (mAbs) can differentiate between these viruses (Yeargan et al 1985;Sinclair et al 1989). Acute EHV-I infections or reactivations of latent infection recur throughout life and may result in a cell associated viraemia and abortion in pregnant mares (Allen and Bryans 1986).…”

Section: Introductionmentioning

confidence: 99%

Distribution of Equid herpesvirus‐1 (EHV‐1) in the respiratory tract of ponies: implications for vaccination strategies

Kydd

Smith

Hannant

et al. 1994

Equine Veterinary Journal

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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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Section: Introductionmentioning

confidence: 99%

Distribution of Equid herpesvirus‐1 (EHV‐1) in the respiratory tract of ponies: implications for vaccination strategies

Kydd

Smith

Hannant

et al. 1994

Equine Veterinary Journal

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“…If the virus is present, CPE is visible within 24-48 h post injection at which time infected cells are harvested and PCR on electron microscopy (EM) used to identify the virus as a herpesvirus. To determine the identity of the virus either PCR (Kirisawa et al 1993), ELISA (Yeargan et al 1985) or DNA fingerprint (Studdert 1983) can be used.…”

Section: Equine Herpesvirus-1 and -4mentioning

confidence: 99%

Abortogenic viruses in horses

Bażanów

Jackulak

Frącka

et al. 2013

Equine Veterinary Education

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Summary Viral causes of abortion include equine viral arteritis (EVA) and infection with equine herpesviruses‐1 and ‐4 (EHV‐1 and EHV‐4). Transmission of equine arteritis virus (EAV) occurs through respiratory, venereal or transplacental routes. Horizontal respiratory transmission of EAV results from exposure to infective nasopharyngeal secretions from acutely infected horses. For this transmission to occur, direct and close contact between horses is necessary. Venereal infection is an efficient method of transmission, with seroconversion of 85 to 100% of seronegative mares bred to virus shedding stallions. Asymptomatic carrier stallions are the essential natural reservoir of equine arteritis virus. Equine herpesviruses‐1 and ‐4 infect a susceptible host, replicate and establish a lifelong latent infection without any associated clinical signs. Reactivation of latent infections can result from factors such as stress and intercurrent disease. The control of these diseases is by implementation of appropriate management and hygiene measures, supplemented by vaccination and, in the case of EVA, by the identification of persistently infected stallions, which can be removed from breeding or continue to be bred to if managed under controlled conditions to prevent the risk of an outbreak of the disease.

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“…For virus isolation, suspensions (10% w/v) of tissue obtained from the aborted fetuses were inoculated onto monolayers of equine fetal kidney cells and the RK-13 cell line. Virus isolates were identified by indirect immunofluorescence, using monoclonal antibodies specific for EHV-1 or -4 (Yeargan et al 1985). Serum antibody titres to EHV-1 were determined by a virus neutralisation test, as described previously by Thomson et al (1976).…”

Section: Laboratory Testsmentioning

confidence: 99%