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N Edington

Publications and source records attributed to N Edington.

At least 55 records · Page 3Linked to original sources

The characterization of equine herpes virus-1-infected cell polypeptides recognized by equine lymphocytes.

Ponies, without evidence of previous exposure to Equine herpes virus-1 (EHV-1), were experimentally infected with EHV-1 subtype 2 and investigated for lymphocyte transformation to virus-infected cell polypeptides, as shown by separation with gel electrophoresis. Animals made significant responses to Western blot fractions that corresponded to molecular weights of approximately 30,000, 40,000-45,000, 60,000-65,000, 80,000-95,000 and 100,000-140,000 MW. These molecular weight ranges correlated with the positions of major EHV-1 subtype 2 glycoproteins that were found at migration distances approximating to 137,000, 111,000, 90,000, 65,000 and 47,000 MW. Responses were also made to a subset of similar points on the subtype 1 profile. Hyperimmune equine serum precipitated numerous infected-cell proteins of both subtypes; in particular the recognition of polypeptides with MW of 142,000, 132,000, 114,000, and 46,000 was in agreement with the mitogenic responses. Labelling with 125I indicated that immunoprecipitated greater than 250,000, 182,000, 142,000, 132,000, 75,000, 46,000 and 32,000/34,000 MW products were exposed on the surface of infected cells.

Animals↗

Neuritis of the cauda equina in the horse.

Ultrastructural lesions of the cranial nerves and their ganglia and the autonomic nervous system from 5 cases of neuritis of the cauda equina in the horse are described. They include lysosomal inclusions within the semilunar, geniculate and sympathetic chain ganglia, granulomatous involvement of the coeliaco-mesenteric ganglion and accumulation of axonal organelles in unmyelinated fibres of the great splanchnic nerve, sympathetic chain and oesophageal vagus.

Animals↗

Rapid diagnosis and characterization of equid herpesvirus 1 using monoclonal antibodies.

Twelve monoclonal antibodies (Mabs) were produced against the attenuated RACH subtype 1 strain of Equid herpesvirus 1. Nine were subtype specific by immunofluorescence or immunoperoxidase, while the other three were against epitopes common to both subtypes. Use of these Mabs allowed isolates to be rapidly and easily subtyped. Immunoblotting indicated that the subtype common Mabs were against viral proteins of MW 140 K and 90 K (VP 9 and 14), while the subtype-specific Mabs were against the glycosylated VP 2 (MW greater than 240 K), and also against VP 12 (MW 110 K) and VP 15 (MW 88 K). Membrane, cytoplasmic, or particulate nuclear patterns of fluorescence were characteristic for each of these proteins. None of the Mabs had neutralising activity but those directed against VP 2 restricted plaque size.

Animals↗

Genetic restriction of cytolysis during equid herpesvirus 1 subtype 2 infection.

Six Welsh Mountain pony foals were experimentally infected with a subtype 2 isolate of Equid Herpesvirus 1 (EHV-1) and subsequently examined for T cell mediated cytotoxicity against both subtypes. Cytotoxicity was not observed at 3 or 7 days after primary exposure but virus-specific, and genetically restricted, cytotoxicity of EHV-1-labelled autologous skin fibroblasts could be demonstrated 7 and 21 days after the animals were given a second exposure to live virus. Killing of subtype 2 antigen-labelled targets was more efficient than subtype 1 coated cells. This finding was paralleled by the observation that virus-neutralizing and complement-fixing antibody levels were subtype specific after the primary infection but after secondary exposure were directed against both subtypes. During primary infection the lymphocyte proliferative response to EHV-1 subtype 2 was not evident at 7 days post infection (dpi) but by 18 dpi was present in all animals. The second exposure produced an earlier (3 dpi) and larger proliferative response which was specific to the infecting isolate. The non-specific proliferative response to Concanavalin A mitogen indicated that virus infection induced a state of activation in circulating lymphocytes.

Animals↗

The proteins of equid herpesvirus 1 (EHV 1) recognised by equine antisera and their ability to promote antibody-dependent cell-mediated cytotoxicity.

Equine sera were used to immunoprecipitate radiolabelled virus-infected cell proteins; subsequent resolution with polyacrylamide gel electrophoresis identified the EHV-1 polypeptides VP 2, 10a, 11, 13, 14, 15, 16, 20, 21 and 23a. The humoral support of ADCC by these sera was examined in vitro. Cytotoxicity could be demonstrated against both subtypes irrespective of the immunising isolate. The implications of these results are discussed.

Animals↗

Endothelial cell infection and thrombosis in paralysis caused by equid herpesvirus-1: equine stroke.

Eight mares were infected with equid herpesvirus-1 subtype 1 isolated from a case of equine paresis. In two mares killed at 4 d.p.i. immunofluorescence showed endothelial cell infection together with thrombosis in the rete arteriosus of the nasal mucosa and also in the spinal cord of one of these mares. Circulating platelet counts in the other six mares fell as early as 2 d.p.i. and remained depressed for seven days. Circulating immune complexes started to appear at 2 d.p.i., reached maximum levels at 10 d.p.i., but were undetectable at 28 d.p.i. Three of the six remaining mares developed varying degrees of inco-ordination at 8 and 9 d.p.i. In the two inco-ordinate mares that were killed at 9 and 10 d.p.i. the haemorrhages in the spinal cord and brain were associated with extensive endothelial cell fluorescence and thrombus formation. Clinical paresis coincided with an increase in circulating complement fixing and neutralising antibodies which in all six mares were higher against the subtype 2 isolate than subtype 1. In five yearlings infected with a subtype 2 isolate of EHV-1 platelet counts remained normal and neither immune complexes nor viraemia, nor inco-ordination were detected.

Animals↗

The lack of effect of inoculation with equine influenza vaccine on theophylline pharmacokinetics in the horse.

Several studies conducted during the past few years have shown that the pharmacokinetics of a variety of drugs may be altered following viral infection or vaccination. The elimination of drugs which are extensively metabolized, such as theophylline, may be prolonged, especially following exposure to RNA viruses such as Type A influenza or similar orthomyxoviruses. The purpose of this study was to determine whether vaccination of horses with equine influenza virus affected pharmacokinetic parameters describing the distribution and elimination of intravenously administered theophylline. Three thoroughbred horses and three ponies were vaccinated with a trivalent vaccine containing inactivated strains of A/Equi 1 (Prague), A/Equi 2 (Miami) and A/Equi 2 (Kentucky 81). Antibody titre, serum interferon concentrations, and the pharmacokinetic parameters t1/2 beta, Vc, Vd(ss), Vd(area) and ClB were measured at various intervals after vaccination. Antibody titre increased substantially in only two animals, while plasma interferon was detectable in low concentrations in four subjects. There was no significant change in any parameter describing the pharmacokinetics of theophylline when measured 2, 6, or 12 days after vaccination. It is suggested that the failure of vaccination to substantially increase plasma interferon concentrations, and thereby alter theophylline elimination, was related to the use of an inactivated viral vaccine, the only type available for vaccination of horses against infection with equine influenza. Regular use of such vaccines, as is required by most Racing Authorities, is therefore unlikely to affect drug withdrawal times.

Animals↗

Innate immunity during Equid herpesvirus 1 (EHV-1) infection.

Intrinsic phagocytosis and killing of C. albicans by equine monocytes and polymorphonuclear leucocytes (PMN) was examined during Equid Herpesvirus 1 (EHV-1) (subtypes 1 or 2) and Adenovirus infections. Monocyte function increased during EHV-1 subtype 2 and Adenovirus infection. Conversely, there was an impairment of monocyte ingestion during EHV-1 subtype 1 infection which was ascribed to virus replication in peripheral blood mononuclear cells. PMN phagocytosis was not decreased in any of the infections studied. The raised levels of haemolytic complement in animals which subsequently developed EHV-1 subtype 1 induced paresis suggested an abnormality of complement turnover. Increased levels of interferon were evident in the nasal secretions of both subtype 1 and subtype 2 infected animals but only subtype 1 virus induced measurable levels of serum interferon. No intrinsic abnormality of interferon production by monocytes or lymphocytes was found.

Adenoviridae Infections↗

Experimental reactivation of equid herpesvirus 1 (EHV 1) following the administration of corticosteroids.

Eight ponies were experimentally infected with equid herpesvirus 1 (EHV 1) (subtype 1). All animals showed clinical and serological evidence of infection and virus was isolated from nasal swabs and leucocytes. These ponies were kept in isolation for a further three months during which time complement fixing antibody decreased at least four-fold. Following immunosuppression with dexamethasone and prednisolone subtype 1 virus was recovered from six of the eight animals within 14 days. Five of these six ponies were viraemic and three of them shed virus in nasal secretions; only four displayed significant rises in complement fixing antibody and only two in neutralising antibody. Clinical abnormalities were not detected during reactivation.

Animals↗

Equine adenovirus 1 isolated from cauda equina neuritis.

Equine adenovirus 1 was recovered after four to six passages from two out of three cases of cauda equina neuritis (CEN) using kidney monolayers. Similar treatment of lumbo-sacral spinal cord from six normal horses did not yield adenovirus. All three cases of CEN had antibodies to the neuritogenic myelin protein P2 while immunofluorescence demonstrated that autologous IgG bound to the myelin of affected nerves. Adenovirus was not detected in neural tissue by immunofluorescence.

Adenoviridae↗

The pathogenicity in mice of respiratory, abortion and paresis isolates of equine herpesvirus-1.

Eleven isolates of equine herpesvirus-1 (subtype 1) all infected the brain following intracerebral inoculation of 2 d.o. mice. Most isolates were from cases of paresis, abortion or respiratory disease in the U.K., but established strains were also included. They divided into two subgroups. The 5 less pathogenic isolates were characterized by being restricted predominantly to the olfactory lobes. The 6 pathogenic isolates included the three known to cause equine paresis and were detected in neurones throughout the brain as well as giving rise to viraemia and infecting bronchial and renal epithelium and lymphoid cells in the spleen. Five respiratory isolates of subtype-2 were not recovered from inoculated mice.

Abortion, Veterinary↗

Herbal medicine.

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Animals↗

Infection of a calf with the enteric coronavirus strain Paris.

A tissue-culture-grown enteric coronavirus infected the whole of the gastrointestinal tract and caused enteritis and diarrhoea in a 10-day-old gnotobiotic Friesian calf. Diarrhoea occurred 2 days after inoculation and excretion of virus in faeces and rectal swabs increased until necropsy at 3 days. Virus growth, as detected by indirect immunofluorescence, virus isolation, and thin section electron microscopy, was most extensive in the epithelium of the colon and rectum at 3 days after inoculation. No virus was detected in other organs or in the pleural, peritoneal and oropharyngeal cavities. The origin and host specificity of this coronavirus is discussed.

Animals↗

Variation in cellular tropism between isolates of equine herpesvirus-1 in foals.

Subtype-1 isolates of Equine herpesvirus-1 (EHV-1) from a quadriplegic horse and from an aborted foetus were compared with each other and with a subtype-2 respiratory isolate. All 3 isolates were detected in the epithelium and macrophages of the respiratory tract. Both the paresis and foetal subtype-1 isolates replicated in the epithelium of the ileum and this correlated with the recovery of virus from faeces in vivo. The paresis subtype-1 isolate also had a predelection for vascular endothelial cells, particularly in the nasal mucosa, but also in the lungs, central nervous system, adrenal and thyroid. In the 9 foals inoculated with the paresis isolate two developed hind limb dysfunction, four developed diarrhoea, and one of these 4 died with an intussusception. The differences between these isolates are discussed in relation to other herpesviruses.

Animals↗

The effect of antibody and complement on the expression of herpesvirus of bovine malignant catarrhal fever in cultured rabbit lymphocytes.

Using indirect immunofluorescence with a hyperimmune calf serum, a virus-induced antigen was demonstrated on the surface of lymphocytes expression intracellular malignant catarrhal fever virus antigens. Antibody to the antigen was also detected in terminal sera of both cattle and rabbits. Antisera did not restrict virus expression in explanted lymph nodes unless they were supplemented with two to four units of lytic complement per ml culture. While human, bovine and guinea pig complements caused immune lysis of infected lymphocytes, rabbit complement was ineffective. The relevance of the findings in the pathogenesis of the lymphoid proliferation caused by MCFV is discussed.

Animals↗

Immune complexes associated with infection of cattle by the herpesvirus of malignant catarrhal fever.

Associated with the fatal lymphoid proliferation induced by the herpesvirus of African malignant catarrhal fever (MCFV) was the deposition of immune complexes comprising immunoglobulin, complement and conglutinin in the kidneys of cattle with terminal pyrexia due to infection with this virus. Such deposits were common in glomeruli and were also seen in renal arteries with an without lesions. Absence of lytic complement and a significant depletion of conglutinin in terminal sera confirmed the activation of complement. However, virus antigen was only rarely detected and virus-specific antibody could not be demonstrated in the deposits. These disparities and the importance of the observations are discussed.

Animals↗