Immunologic Relationship between JM and JMV Leukosis Strains and Herpesvirus of Turkeys

Hamdy, Farouk; Sevoian, Martin

doi:10.2307/1589146

Cited by 6 publications

(6 citation statements)

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“…This result confirms the findings of Witter et al (1975) and Stephens etal. (1976), however, it is inconsistent with recent reports of other authors (Spencer etal., 191 A, 1976;Yoon and Kenyon, 1975;Yoon et al, 1976;Hamdy and Sevoian, 1973;Hong and Sevoian, 1974;Sevoian, 1974, 1975) who have found JMV to be associated with MDV antigenicity. Because of the origin of JMV from a MD tumour the isolated cells were probably infected with MDV, and it is possible that the level of MDV infection decreased only gradually during the great number of chicken passages until the virus disappeared completely.…”

Section: Discussionmentioning

confidence: 99%

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Propagation and assay of virulent and attenuated JMV Marek's disease‐associated tumour cells

Bülow¹,

Weiland²

1977

Avian Pathology

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SUMMARYJMV tumour cells were shown to cause a lethal lymphoblastic leukaemia in young chickens as well as in chicken embryos. The incubation period was very short but dose-dependent. Chickens died in 4 to 12 days, embryos in 7 to 14 days, after inoculation. Embryo-passaged attenuated JMV (JMV-A) caused the same lesions in embryos as virulent JMV. The dose-response relationship depended on the route of inoculation and on the quality of the tumour cell preparation. Intramuscular (i.m.) inoculation of leukaemic blood or embryo lymphoblasts provided the most satisfactory response. Intraperitoneal (i.p.) inoculation and lymphoblastic chicken spleens as a source of JMV were definitely less suitable. The doseresponse curves obtained in yolk sac-inoculated embryos were similar to the curves obtained by i.m. inoculation of chickens. Only 4 to 10 lymphoblasts were needed per lethal dose (50%) in chickens and 50 to 80 in embryos.The pathogenicity and antigenicity of JMV and JMV-A were strictly cellassociated. No Marek's disease (MD) virus or any other avian virus could be detected, either by various virus isolation procedures, or by serological methods. Contact transmission of JMV to other chickens did not occur.Antibodies against surface antigens on JMV lymphoblasts were detected in JMV and JMV-A chicken hyperimmune sera. These sera reacted against MD lymphoblastoid cell lines (HPRS-1 & 2, MSB-1) as well as MSB-1 antiserum, but all sera reacted also against thymus lymphocytes from normal chickens. The results of absorption tests suggested that the surface antigens of JMV lymphoblasts and of the tested cell lines were not identical. The majority of tumour cell surface antigens appeared to represent genetically specific histocompatibility or lymphocyte antigens. A common MD tumourassociated surface antigen (MATSA) could not be identified serologically (FA test) on the tumour cells studied.

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Section: Discussionmentioning

confidence: 99%

“…Sevoian (1974, 1975) reported on a possible cross-protection between JMV or JMV-A and MDV or HVT which was supported by results of serological assays (Hamdy and Sevoian, 1973;Hong and Sevoian, 1974;Shieh and Sevoian, 1975).…”

Section: Introductionmentioning

confidence: 89%

Propagation and assay of virulent and attenuated JMV Marek's disease‐associated tumour cells

Bülow¹,

Weiland²

1977

Avian Pathology

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“…Studies designed for the biological characterisation of JMV have revealed that virulent as well as attenuated JMV lymphoblasts (JMV, JMV-A) were lacking in rescuable virus (Witter et ai, 1975;Stephens etal, 1976;Bülow and Weiland, 1977). This is inconsistent with the results of other authors who found Marek's disease virus (MDV) or an unspecified herpesvirus associated with JMV (Hamdy and Sevoian, 1973;Hong and Sevoian, 1974;Shieh and Sevoian, 1974;Spencer et al ,1974Spencer et al , , 1976Yoon andKenyon, 1975;Yoon et al, 1976).…”

Section: Introductionmentioning

confidence: 94%

Cross‐protection between JMV Marek's disease‐derived tumour transplant, Marek's disease and Turkey herpesviruses

Bülow¹

1977

Avian Pathology

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Cross-protection tests were conducted using attenuated JMV (JMV-A) Marek's disease-derived lymphoblasts, glutaraldehyde-treated JMV tumour cells, attenuated Marek's disease virus (MDV, strain HPRS-16/att) and turkey herpesvirus (HVT, strain FC126) as vaccines, and virulent JMV and MDV (HPRS-16) for challenge. The JMV and JMV-A preparations were free of MDV, leukosis and reticuloendotheliosis viruses. Vaccination of chickens with attenuated MDV or with HVT provided good protection against both JMV lymphoblastosis and Marek's disease (MD). In one experiment HVT (cell-free) caused a better resistance to JMV than to MD. Inoculation of JMV-A always resulted in a 100% resistance to virulent JMV. However, JMV-A did not induce any appreciable resistance to MD, even when the birds were challenged with MDV by contact exposure. Control experiments revealed that high doses of normal lymphocytes from uninfected chickens also had a protective effect against JMV. The 50% protective dose varied from 10(7) to 10(8) lymphocytes. JMV tumour cells inactivated by glutaraldehyde were used in different experiments but rarely caused a clear-cut protection against virulent JMV. The results of this study suggested that a one-way relationship exists in vivo between HVT or MDV and JMV lymphoblastic leukaemia. However, resistance induced against JMV tumour cells appeared to be related to histocompatibility antigens at least as much as to tumour-specific cell surface antigens. The results obtained failed to provide clear evidence for or against vaccinal resistance to MDV being dependent on the action of a common Marek's disease tumour-associated surface antigen (MATSA) additional to the immune response to viral antigens.

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“…Dissociated kidney cells were washed twice in maintenance media and seed-d in Falcon Petri dishes (65 mm) at a cell concentration of 2 x lo8 cells per plate. The cells were grown in Medium 199, supplemented with 1 % fetal calf serum, 2% tryptose phosphate broth and antibiotics (Hamdy and Sevoian, 1973). After 7 days of cultivation, when virus-induced plaques were visible, the monolayers were harvested by trypsinization and washed twice.…”

Section: Jm Virusmentioning

confidence: 99%

“…The in vivo studies concentrated on the role of the macrophage in response to viral infection and to the tumorigenic process by selectively depressing macrophage functions with antimacrophage serum (Unanue, 1968) (Hamdy and Sevoian, 1973). After 7 days of cultivation, when virus-induced plaques were visible, the monolayers were harvested by trypsinization and washed twice.…”

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confidence: 99%

The role of the macrophage in Marek's disease: In vitro and in vivo studies

Haffer

Sevoian

Wilder

1979

Intl Journal of Cancer

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Macrophages form S- and K-strain Leghorn chickens, susceptible and restant to Marek's disease (MD) respectively, were studied to determine the macrophage contribution to the dynamics of MD infection, tumorigenesis and genetic resistance to this disease. In vitro studies demonstrated that macrophages from bothstrains were similar in their responses toward JM strain of Marek's disease virus (MDV) and JM-1 tumor cells. Macrophages were observed to phagocytize JM virus, but the interiorized virus was not seen to replicate within the macrophage or induce antigenic changes of the cell membrane. Clearance of JM-1 tumor cells was by both cytolytic and phagocytic mechanism. In vivo selective suppression of macrophage functions by antimacrophage serum or trypan blue inoculations resulted in significantly elevated viral titers and increased tumorigenesis, as compared to infected, non-suppressed or non-infected control groups. Results from this study indicate that genetic susceptibility or resistance to MD, as exhibited by S- and K-strain chickens, respectively, is not controlled at the macrophage level. The role of the macrophage in MD infection appears to be specifically surveillance.

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Immunologic Relationship between JM and JMV Leukosis Strains and Herpesvirus of Turkeys

Cited by 6 publications

References 5 publications

Propagation and assay of virulent and attenuated JMV Marek's disease‐associated tumour cells

Propagation and assay of virulent and attenuated JMV Marek's disease‐associated tumour cells

Cross‐protection between JMV Marek's disease‐derived tumour transplant, Marek's disease and Turkey herpesviruses

The role of the macrophage in Marek's disease: In vitro and in vivo studies

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