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Biomedical subjects

R L Witter

Publications and source records attributed to R L Witter.

At least 73 records · Page 4Linked to original sources
PubMed1977

Isolation from a transmissible lymphoid tumour (TLT) lymphoblastoid cell line of a herpesvirus similar to Marek's disease virus.

A chicken lymphoblastoid cell line (TLT)-6855 originally established from an avian oncornavirus-induced lymphoma (Siegfried and Olson, 1972) was studied for the presence and expression of Marek's disease virus (MDV) genome. By nucleic acid hybridization a significant amount of MDV DNA was found in this cell line. This virus DNA, however, was not expressed in either virus-specific intracellular or membrane antigens or the MD-associated tumour-specific surface antigen (MATSA). Moreover, MDV-specific antigens could not be activated in this cell line by treatment with 5-IdUrd. In several experiments, when chickens were inoculated with the cell line a herpesvirus was repeatedly isolated from the kidneys. This herpesvirus was antigenically similar to MDV but was low in oncogenicity for chickens.

Animals↗
PubMed1977

Role of the major histocompatibility complex in resistance to Marek's disease: restriction of the growth of JMV-MD tumor cells in genetically resistant birds.

B21 is associated with resistance to Marek's disease (MD). Forty populations of chickens from all over the world were examined for the presence of the B21 allele. B21 was found in twelve of these populations and it's presence was confirmed by GVH testing in all ten populations which were tested. The populations in which B21 was detected represent the extreme production types of the species and include the progenitor of the species, the Red Jungle Fowl. Our studies suggest that B21 may have strong survival value for the species. An allogeneic transplantable lymphoma of MD, the JMV tumor cell line, grows more slowly in MD resistant (B21/B21) chicks than in MD susceptible (B2/B2) chicks. This is the first direct evidence that genetic resistance to MD may involve an active (immunological?) restriction of tumor cell growth. JMV cells were further characterized as a transplant of B1 carrying lymphoblastoid cells, an allele which may be associated with susceptibility to MD.

Animals↗
PubMed1977

Reduced incidence of Marek's disease gross lymphomas in T-cell-depleted chickens.

Chickens of line 7, highly susceptible to Marek's disease (MD), were depleted of T-cells by neonatal thymectomy, total-body gamma-irradiation, and multiple injections with antithymocyte serum. In two replicate experiments, significantly fewer gross lymphomas were present in T-cell-depleted chickens than in intact or in T-cell-depleted, reconstituted hatchmates; these findings provided evidence that T-cells may be the principal target for MD virus (MDV) transformation, T-cell depletion was not complete, and the presence of microscopic lesions in T-cell-depleted chickens was attributed to residual T-cells. Ten lymphomas from intact chickens and 2 lymphomas from a T-cell-depleted chicken were examined for cellular composition. All lymphomas consisted predominantly of T-cells. The results of this and other published studies indicated that T-cells may have a dual role in MD; They may serve as a target for lymphoma formation by MDV and also may participate in immune surveillance against the disease in resistant chickens.

Animals↗
PubMed1976

Characteristics of JMV Marek's disease tumor: a nonproductively infected transplantable cell lacking in rescuable Virus.

Cells of the JMV Marek's disease (MD) tumor, originally produced by rapid serial passage of MD lymphoma cells in chickens, were characterized to determine whether they were of host or donor origin and to ascertain certain virus-host cell interrelationships. Differences noted in blood group B surface alloantigens between tumor cells and host lymphocytes indicated a probable nonhost origin (i.e., transplantability) of the tumor. JMV spleen tumors contained predominantly large lymphoblasts bearing MD tumor-associated surface antigen. DNA from JMV tumor cell suspensions hybridized significantly with MD virus cRNA, which indicated that JMV cells contained at least a portion of the MD virus genome. No MD virus was rescued from JMV tumors by techniques suitable for rescue of virus from MD lymphomas. The JMV tumor cells were also devoid of MD virus-specific antigens. These properties differed markedly from those of MD lymphoma cells and make the JMV tumor cell a unique, potentially valuable, tool for further study of oncogenic herpesvirus infection and tumor immunity in the chicken.

ABO Blood-Group System↗
PubMed1976

Natural mechanisms of controlling lymphotropic herpesvirus infection (Marek's disease) in the chicken.

Four categories of natural resistance phenomena against Mareks disease in chickens, i.e., maternal antibody, age resistance, genetic resistance, and natural immunization, are described. In nature, these forms of resistance probably act in concert through comlex interrelationships. The mechanisms are not well understood but include humoral immunity (maternal antibody), cell-mediated immunity, and possibly other mechanisms. The possible role of newly discovered tumor-specific antigens in cell-mediated immunity against Marek's disease lymphomas is discussed.

Age Factors↗
PubMed1975

Oncogenesis by Marek's disease herpesvirus in chickens lacking expression of endogenous (gs, chick helper factor, Rous-associated virus-O) and exogenous avian RNA tumor viruses.

Chickens free of exogenous avian leukosis virus (ALV) infection, replicating endogenous ALV (Rous-associated virus-O), gs antigen, and chick helper factor were fully susceptible to induction of Marek's disease (MD) by ALV-free MD viruses. Dual infection with Rous-associated virus-2 and MD virus did not significantly alter the character of the MD lesions. Thus exogenous ALV infection was not requisite for MD virus-induced oncogenesis. Although participation of endogenous RNA tumor virus genes in MD lesion induction could not be excluded, expression of such genes in MD tumors as gs antigen was not established.

Animals↗
PubMed1975

Low oncogenic potential of avian endogenous RNA tumor virus infection or expression.

Of chickens either spontaneously producing or exogenously infected in ovo with Rous-associated virus, type O (RAV-O), an endogenous virus of the chicken, only 1 died with lymphoid leukosis (LL), the most common neoplasm associated with the leukosis-sarcoma virus group. Because the chickens were not kept in strict isolation, it could not be assumed that the one LL was induced by RAV-O. In contrast, RAV-1-infected chickens from the same lines had a high incidence of LL and other neoplasms. Over 800 chickens of several inbred lines were maintained in plastic isolators free of exogenous avian leukosis-sarcoma virus infection for from 500 to nearly 1,000 days of age. No LL was observed, even though some lines are known to produce RAV-O spontaneously or to express inherited gs antigen. Three neoplasms of unknown etiology were observed, but none generally associated with leukosis virus infection. We concluded that avian endogenous virus expression had little, if any, oncogenic potential, and that exogenous avian leukosis viruses were responsible for most naturally occurring neoplasms.

Animals↗
PubMed1975

Properties of a chicken lymphoblastoid cell line from Marek's disease tumor.

Properties of a chicken lymphoblastoid cell line (MSB-1) from a Marek's disease tumor were studied. The cell line grew well at 41 degrees C in medium RPMI-1640 supplemented with 10% bovine fetal serum and had a doubling time of 8-12 hours. Cells grown in stationary suspension culture did not attach to the vessel and had the morphology of typical lymphoblasts. At 37 degrees C, the cell line grew initially but ceased to divide after several subcultures. In the subcultures maintained for 48-72 hours, 1-2% of the cells produced Marek's disease virus (MDV)-specific intracellular and mambrane antigens and contained herpesvirus particles when examined by the electron microscope. Cocultivation of these cells with duck or chicken embryo fibroblast cultures resulted in transfer of infection and production of microplaques typical of MDV. Peripheral nerve lesions and lymphoid tumors characteristic of Marek's disease were caused by inoculation of susceptible chicks with MSB-1 cells or duck cells infected with strain BC-1 of MDV recovered from the MSB-1 cell line. No specific tumors were produced at the site of inoculation, and infection was readily transmitted to cagemates. Tumors were also produced in the skeletal muscles and seemed to be largely virus induced. MSB-1 cell line was free of C-type virus particles.

Animals↗
PubMed1975

The effect of B-cell immunosuppression on age-related resistance of chickens to Marek's disease.

Chickens were bursectomized by cyclophosphamide treatment at hatching. At 8 or 9 weeks of age, bursectomized and unbursectomized hatchmates, free from prior infection, were challenged with pathogenic Marek's disease virus. Oncogenicity of the virus inoculum was confirmed by inoculating 1-day-old susceptible chickens. At the time of virus challenge, blood cells from the cyclophosphamide-treated chickens were able to mount a vigorous graft-versus-host reaction in allogeneic embryos. This ability indicated that the thymus function was intact. There were no significant differences in Marek's disease response of bursectomized and unbursectomized chickens, in spite of a severe defect in the bursa-dependent functions in the bursectomized chickens. Some bursa-deficient chickens had non-proliferating, presumably regressing lesions in peripheral nerves. Because these lesions lacked plasma cells, it was concluded that the plasma cell may not play a functional role in recovery from Marek's disease.

Aging↗
PubMed1975

Demonstration of a tumor-associated surface antigen in Marek's disease.

Surface antigenic markers were detected on three classes of Marek's disease (MD) tumor cells, i.e., MD lymphoma cells, cultured cells of the MSB-1 lymphoblastoid cell line, and JMV lymphoblastic leukemia cells, by indirect membrane immunofluorescent staining with serum from chickens immunized with JMV cells or from rabbits immunized with MSB-1 cells. This surface antigen was not detected on normal chicken lymphocytes, RPL-16 tumor cells (tranedormed by an avian RNA virus, or MD virus-infected fibroblasts that were positive for viral membrane antigen (MA). Furthermore, the surface antigen appeared unrelated to embryonic or histocompatibility antigens. This antigen is provisionally designated as a Marek's disease tumor-associated surface antigen (MATSA). The MATSA's on JMV, MSB-1 and MD lymphoma cells were related but not identical as demonstrated by antiserum titration, absorption and blocking tests with homologous and heterologous systems.

Analysis of Variance↗
PubMed1973

Pathogenesis of Marek's disease in old chickens: lesion regression as the basis for age-related resistance.

Chickens of various age levels, free from prior infection, were simultaneously exposed to Marek's disease virus, and the response of each age group was recorded. Four- and 20-week-old chickens of lines 15x7 and CM (commercial source) had substantial resistance to mortality and gross lesions. In contrast, in line 7, which was tested at 1-day, 2-, 4-, 8-, 12- and 16-week age levels, 4-week-old chickens were fully susceptible to clinical Marek's disease (MD), although resistance was demonstrated at 8-week and older age levels. Genetically resistant chickens of line 6 maintained their resistance at all age levels tested. Pathogenesis of MD was compared in 12-week-old and 1-day-old chickens of line 15x7. Within the 1-day-old group, 23% of the chickens died because of MD, whereas there were no deaths in the 12-week-old group. Both groups developed viremia although duration, incidence, and levels of virus in the 1-day-old group were higher than in the 12-week-old group. Although initially the 12-week-old group responded by producing higher levels of antibody, the long term incidence of agar gel precipitin, immunofluorescent, and virus neutralization antibody in the two groups was similar. Gross and microscopic lesions of MD developed in both groups, but lesions regressed in the 12-week-old group and persisted in the 1-day-old group. It was concluded that age resistance to MD was expressed through lesion regression.

Age Factors↗
PubMed1972

Efficiency of commercial air filters against Marek's disease virus.

In a series of 10 replicate trials with susceptible chickens as indicators of the presence of virus in the air, filter B(1) (Dri Pak, American Air Filter Co.), which has a dust spot rating of 93 to 97%, and filter C (Astrocel), with a dioctyl phathalate aerosol rating of over 99%, completely removed Marek's disease virus (MDV) from highly contaminated air. However, air passed through filter B(2) (Duracel), with a dust spot rating of 34 to 45%, remained infectious. Thus, an air filter with a dust spot rating of over 93% will effectively remove MDV from the air. The smallest infectious particles in the air are estimated to be greater than 0.3 mum in diameter.

Air Microbiology↗