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Biomedical subjects

H W Reid

Publications and source records attributed to H W Reid.

At least 73 records · Page 4Linked to original sources
PubMed1991

Recovery of a herpesvirus from a roan antelope (Hippotragus equinus).

A herpesvirus was recovered in culture from the cells of a roan antelope (Hippotragus equinus) following cryopreservation in DMSO and it is thought that the DMSO may have been involved in reactivation. The virus was shown to be antigenically related to alcelaphine herpesvirus-1 (AHV-1) of wildebeest and ovine herpesvirus-2 (OHV-2) of domestic sheep (formerly designated the sheep-associated agent of malignant catarrhal fever (MCF]. Cloned DNA fragments of AHV-1 and OHV-2 cross hybridised with DNA prepared from cells infected with the roan antelope virus and the intensity of reaction suggested that this virus was more closely related to AHV-1 than is OHV-2. The virus represents the third gamma herpesvirus isolated from large African antelope and should be provisionally designated hippotragine herpesvirus-1. On inoculation into rabbits the virus induced malignant catarrhal fever indicating that roan antelope should be considered as a possible source of infection.

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PubMed1991

Derivation of a DNA clone corresponding to the viral agent of sheep-associated malignant catarrhal fever.

Malignant catarrhal fever is a fatal lymphoproliferative and degenerative disease of ruminants. One causative agent is the gammaherpesvirus alcelaphine herpesvirus 1 (AHV-1), which produces no disease in its natural host, the wildebeest (Connochaetes species). Epidemiological evidence implicates sheep as the carrier of a similar virus. However, attempts to culture this virus from sheep or from animals affected with sheep-associated malignant catarrhal fever (SA-MCF) have failed. Lymphoblastoid cells have been propagated from cattle, deer and rabbits with SA-MCF. Although these cells show no evidence of viral particles or antigens, hybridisation experiments now show that they contain DNA sequences homologous to those of AHV-1. A genomic library was constructed from one of these lymphoblastoid cell lines and a clone identified which hybridised to cloned AHV-1 DNA. The authors believe that this clone contains part of the SA-MCF viral genome, and that the SA-MCF virus and AHV-1 are closely related gammaherpesviruses.

Animals↗
PubMed1991

Phenotypic analysis of lymphoblastoid cell lines derived from cattle and deer affected with "sheep-associated" malignant catarrhal fever.

Established lymphoblastoid cell lines with natural killer cell-like activity have been derived from cattle and deer affected with malignant catarrhal fever. They were examined phenotypically using monoclonal antibodies chosen for their cross-reactivity with peripheral blood lymphocytes from these species. Cell lines established from three of four cattle were identified as cytotoxic/suppressor lymphocytes (CD4-/CD8+/T19-) whilst the other was shown to be of the helper cell phenotype (CD4+/CD8-/T19-). Two other cell lines, one derived from a red deer and the other from a Père David's deer, were both CD4-/CD8-/T19. All of the lines examined expressed a T cell receptor (CD2+).

Animals↗
PubMed1991

Response of efferent lymph and popliteal lymph node to epidermal infection of sheep with orf virus.

Functional and phenotypic changes in the cell populations were monitored in the popliteal efferent lymph of sheep following experimental epidermal infection with orf virus. In another group of sheep, cells from the popliteal lymph node draining the site of infection were similarly monitored and compared with the cells from contralateral popliteal and mesenteric lymph nodes. All sheep showed serological evidence of previous exposure to orf virus. Following infection, anti-orf antibody titres rose and efferent lymphocyte and blast cell output increased. Interferon-like activity was detected in efferent lymph early after orf virus but not mock infection. Lymphocytes from the draining popliteal lymph node showed antigen-specific lymphoproliferation on Days 3-7 while cells in the efferent lymph demonstrated proliferative activity on Days 4-6. The requirement for exogenous antigen-presenting cells in the culture of efferent lymphocytes varied between individual sheep. The culture supernatant from proliferating lymph node cells contained interferon-like activity but no anti-orf antibodies, the reverse of that from cultured efferent lymphocytes, perhaps indicating a different reactive T cell population. During the course of the experiment there was an increase in the percentage of efferent lymphocytes expressing MHC Class II antigens and surface immunoglobulins, the latter being recorded as a double peak. The short-term nature of the local T cell response may in part explain the incompleteness of immunity to orf virus in sheep.

Animals↗
PubMed1989

Immune response of lambs to experimental infection with Orf virus.

A group of six specific pathogen free (SPF) lambs were infected epidermally with Orf virus. Seven weeks later they were reinfected. For a period of 4 weeks after each inoculation they were observed clinically and blood was collected for analysis of virus specific antibody measured by ELISA and peripheral blood lymphocyte (PBL) proliferative response to various viral antigens. After the primary infection all animals showed clinical signs of Orf, namely vesicle formation which became pustular followed by scabbing; this steadily became heavier prior to shedding and the resolution of the infection by about 4 weeks. The severity of infection varied within the group. Little lymphoproliferative activity was recorded during the primary infection, although five/six test animals had positive lymphoproliferative responses to an sodium dodecyl sulphate (SDS) solubilised scab purified Orf virus preparation at some point between days 7 and 14 after inoculation. All animals seroconverted to Orf virus, lymphoproliferative activity always preceding specific antibody detection. Resolution of the secondary infection was very rapid. Vesicles were visible by day 2 after inoculation which became pustular followed by scab formation and resolution in the majority of animals by day 8. All animals showed a significant (greater than four-fold) rise in specific antibody titre following secondary inoculation. The proliferative activity of PBL's was much greater than that recorded for the primary infection although the magnitude of this response varied greatly between individuals.

Animals↗
PubMed1989

Preliminary characterization of the alcelaphine herpesvirus 1 genome.

Alcelaphine herpesvirus type 1 (AHV-1) is a causative agent of the fatal lymphoproliferative disease malignant catarrhal fever in deer and cattle. The genomes of the attenuated WC11 isolate and the virulent C500 isolate have been studied. The genome of WC11 comprises a region of unique DNA of approximately 130 kbp, which has a G + C content of 50%, and approximately 30 kbp of additional tandem direct repeat sequences with G + C content of 72%. WC11 possesses a major repeat sequence of 950 bp interspersed with a small number of related sequences of different length; these sequences are probably terminal in location. DNA from the C500 isolate has a similar restriction profile to that of WC11 in the unique region, but only one repeat sequence of 1050 bp is present. We propose, on the basis of biological and structural properties, that AHV-1 be included within the gamma 2 group of herpesviruses of which herpesvirus ateles is the prototype.

Animals↗
PubMed1989

Antibody to alcelaphine herpesvirus-1 (AHV-1) in hamsters experimentally infected with AHV-1 and the 'sheep-associated' agent of malignant catarrhal fever.

Malignant catarrhal fever was induced in four groups of hamsters by the inoculation of cells infected with either the C/500 isolate of alcelaphine herpes-virus-1 (AHV-1) or the sheep-associated agent derived from cattle, red deer or Père David's deer. Using an indirect immunofluorescence assay, antibody to AHV-1 was detected in sera of clinically affected animals of all four groups. The reaction of sera from hamsters affected with malignant catarrhal fever induced by AHV-1 caused diffuse cytoplasmic staining while that from sera of hamsters with the sheep-associated form of the disease stained particulate nuclear antigens. Tests employing three other bovid herpesviruses were negative and no reaction was found with sera from normal hamsters. These studies provide convincing evidence that a virus antigenically related to AHV-1 is the cause of sheep-associated malignant catarrhal fever and that the same virus probably causes this form of the disease in both cattle and deer.

Animals↗
PubMed1989

Isolation and characterisation of lymphoblastoid cells from cattle and deer affected with 'sheep-associated' malignant catarrhal fever.

Cells with the histological and ultrastructural characteristics of large granular lymphocytes (LGL) have been obtained in culture from both cattle and red deer (Cervus elaphus) reacting with 'sheep-associated' malignant catarrhal fever (MCF). Such cells have been derived from thymus, lymph node and spleen suspensions as well as from cerebrospinal fluid cells and cultured cornea. On most occasions their presence was observed only transitorily but by providing the cells with feeder monolayers and, or, interleukin-2, several lines were maintained indefinitely, and some became independent of these factors after prolonged culture. A similar cell line was also derived from a Père David's deer affected with MCF at Whipsnade zoological park. Functionally, cultured LGL were cytotoxic to both primary cell cultures and cell lines and their cytotoxicity was not restricted to histocompatible target cells. These findings suggest that the cultured cells have natural killer cell-like activity and that they are important targets for the agent of MCF in cattle and deer. One cell line derived from a red deer transmitted the disease but none of the cells generated from cattle did.

Animals↗
PubMed1989

Lymphocyte subpopulations in the blood of sheep persistently infected with border disease virus.

The surface phenotypes of peripheral blood lymphocytes in groups of lambs and adult sheep persistently infected with Border disease virus (P-I BD) were compared with those of healthy controls. The proportion and number of lymphocytes bearing surface immunoglobulin (sIg+) and expressing class II MHC antigen (B cells) were significantly increased. A significant increase in CD1+ lymphocytes was also evident. Conversely, the proportion of T lymphocytes in P-I BD lambs was reduced. A marked reduction in the proportion of circulating lymphocytes expressing class I MHC antigen was also observed. These findings were not affected by differences in the strain of the virus responsible for the persistent infection.

Aging↗
PubMed1988

The pathology of "sheep-associated" malignant catarrhal fever in the hamster.

Lesions induced in hamsters by inoculation with the "sheep-associated" agents of malignant catarrhal fever (SA-MCF) isolated from a red deer (Cervus elaphus), designated D/1 and of bovine origin (C/2), are described. Clinical signs in hamsters inoculated with the D/1 isolate occurred as early as 13 days after infection although the mean incubation period in animals that developed signs was 27 days. Increased numbers of polymorphonuclear leucocytes were present in the blood of clinically affected hamsters. Gross lesions included erosions of epithelium in the buccal cavity, haemorrhage of the forestomach, dilated fluid-filled intestines and enlargement of the mesenteric lymph node. Microscopic lesions were widespread throughout the body but had a predilection for epithelial surfaces. They consisted of hyperplasia of certain lymph nodes, vasculitis and interstitial accumulations of mononuclear cells of lymphoid appearance in non-lymphoid tissues. Cytolysis was also seen. Lesions produced by the C/2 isolate were similar and both isolates produced disease comparable with that seen in naturally occurring cases in cattle and deer. It is suggested that disease might arise through a dysfunction of the immune system following infection of host large granular lymphocytes by the SA-MCF agent, in a way similar to that suggested for the rabbit.

Animals↗
PubMed1988

Transmission of wildebeest-associated and sheep-associated malignant catarrhal fever to hamsters, rats and guinea-pigs.

Wildebeest-derived malignant catarrhal fever (WD-MCF) was transmitted to hamsters, rats and guinea-pigs by inoculation of rabbit lymphoid cells infected with alcelaphine herpesvirus-1, strain C-500. Sheep-associated MCF (SA-MCF) was transmitted to hamsters by inoculation of lymphoid cells from rabbits affected with SA-MCF derived from deer. Mice were refractory to both forms of the disease. With both forms of MCF, the incubation period during initial transmission varied from 21 to 90 days and disease was readily passaged in rodents by inoculation of live lymphoid cells. Clinical signs in hamsters most closely resembled those described for naturally occurring MCF. Results given here and in two following papers indicate that rodents are useful models to study the aetiology and pathogenesis of both forms of MCF.

Animals↗
PubMed1988

The pathology of wildebeest-associated malignant catarrhal fever in hamsters, rats and guinea-pigs.

Lesions typical of malignant catarrhal fever were found in hamsters, rats and guinea-pigs inoculated with a rabbit-passaged strain (C-500) of alcelaphine herpesvirus-1. Lesions found during primary passage included proliferation of lymphoid tissues, multisystemic mononuclear cell infiltrates, vasculitis and necrosis, especially in the alimentary tract. The character, severity and distribution of lesions remained stable in affected hamsters during serial passage of disease, whereas lympho-proliferation became dominant in rats. The lesions in rats typically affected lymph nodes, heart and kidney and appear similar to those caused by oncogenic herpesviruses. Because rodents are susceptible to malignant catarrhal fever, the prospect is advanced that they can be used to elucidate the pathogenesis of both lymphoproliferative and cytolytic aspects of the disease.

Animals↗
PubMed1988

Studies of the pathogenesis of orf virus infection in sheep.

Damage to the skin is essential for the establishment of orf virus infection and the development of typical lesions. However, analysis of the pathogenesis of experimental lesions induced by viral challenge of mildly abraded skin, indicated that the virus does not establish in the damaged epidermis, but replicates in the cells of an underlying replacement epidermal layer derived from the walls of the wool follicles. The skin reaction consists of a cellular response with necrosis and sloughing of the affected epidermis and underlying stratum papillare of the dermis. Healing is then completed by the formation of a third epidermis derived from the deeper portions of the wool follicles. Previous cutaneous infection did not prevent reintroduction of the disease, even on the same area of skin although the lesions were less severe and persisted for a shorter period.

Animals↗
PubMed1987

A disease resembling louping-ill in sheep in the Basque region of Spain.

A clinical syndrome resembling louping-ill which primarily affects lambs and yearlings in the Basque region of Spain is described. The disease has been observed for several years during May and June after the sheep flocks have been taken to the mountain grazings where the sheep tick (Ixodes ricinus) is known to occur. Examination of the brain from one of the affected animals revealed histological changes indistinguishable from those caused by louping-ill virus. In addition antibody that reacted with louping-ill virus antigen was detected in the serum of 57 per cent of the sheep tested from the affected flocks but in only 0.8 per cent of sera from flocks free of the disease. These preliminary results suggest that louping-ill or a related tick-borne virus is responsible for ovine encephalomyelitis in Spain.

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