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Biomedical subjects

B W Calnek

Publications and source records attributed to B W Calnek.

At least 37 records · Page 2Linked to original sources
PubMed1982

Syngeneic and allogeneic cell-mediated cytotoxicity against Marek's disease lymphoblastoid tumor cell lines.

Cell-mediated cytotoxicity (CMC) of lymphocytes obtained from chickens infected with Marek's disease (MD) virus against allogeneic MD lymphoblastoid cell lines has been reported by several research groups. Recently, we established a number of cell lines from MD tumors obtained from highly inbred chickens and characterized for major and minor histocompatibility antigens. Allogeneic versus syngeneic CMC was studied using those cell lines and lymphocytes obtained from chickens 6-8 days post infection with SB-1, a non-oncogenic MD virus. Allogeneic cytotoxicity could be easily demonstrated, while syngeneic cytotoxicity was a rare event. However, increase of the CMC assay period from 4 to 8 h did enhance syngeneic cytotoxicity. Cold inhibition assays demonstrated that the allogeneic cytotoxicity was directed against alloantigens present on spleen lymphocytes sharing the same major histocompatibility antigens as the target cells. Cytotoxicity was not influenced by the sex of either target or effector cells or by the level of virus infectivity of the effector cells.

Animals↗
PubMed1982

In vitro infection of lymphocytes with Marek's disease virus.

Suspension cultures of splenic lymphocytes, incubated at 41 degrees C, became infected with Marek's disease virus (MDV) following exposure to a) other infected lymphocytes, b) infected chicken kidney monolayer cultures, or c) cell-free MDV. Both viral antigen expression and virus isolation could be demonstrated after more than 40 passages made by the addition of fresh spleen cells at 2- to 3-day intervals. Susceptibility of spleen cells from bursectomized chickens was markedly lower than that of cells from intact birds. Furthermore, when spleen cell suspensions were depleted of cells having characteristics of bursa-derived cells, e.g., those with surface IgM, Fc receptors, or ability to adhere to nylon wool, the susceptibility of the cell suspension was diminished. Enrichment of the suspension with cells having those features enhanced overall susceptibility. The target cells for virus infection in vitro also were shown to be nonphagocytic, to be of low or medium density, and to bear Ia-like antigen. In vitro susceptibility to infection of spleen cells did not correlate with the genetic susceptibility of the donor to Marek's disease.

Animals↗
PubMed1982

Marek's disease vaccines.

Marek's disease (MD) vaccines have been in almost universal use since the early 1970's and constitute the first effective practical means for the control of any neoplastic disease in man or animals. Five types have been described: 1) attenuated variants of oncogenic strains (Serotype 1) of Marek's disease virus (MDV) produced by serial passage in cultured cells; 2) naturally nononcogenic MDV strains (Serotype 2); 3) nononcogenic herpesvirus from turkeys (HVT, Serotype 3); 4) inactivated cells or cell membrane components from infected cell cultures containing viral-associated antigens; 5) inactivated cells or membrane components from lymphoblastoid MD tumor cell lines containing presumed tumor-associated antigens. HVT vaccines, in either cell-associated or cell-free form, are most frequently used for vaccination of commercial flocks. Both cell-mediated and humoral immune responses are mounted and each may contribute to vaccinal immunity. Probably the most significant responses are against the early (cytolytic) phase of MDV infection, although vaccines apparently also induce a response against tumor-specific antigens as well.

Animals↗
PubMed1982

Surface antigens on Marek's disease lymphoblastoid tumor cell lines.

A total of 32 Marek's disease virus (MDV)-induced cell lines, 1 avian leukosis virus-induced cell line, and 1 reticuloendotheliosis virus (REV)-induced lymphoblastoid cell line were investigated for the presence of Fc receptors, surface IgM, and Ia-like antigen. Surface IgM and Fc receptors could not be demonstrated on any of the cell lines. Ia-like antigen was detected on all MDV-induced cell lines and on the 1 REV-induced cell line. Ia-like antigen was unrelated to other antigens reported to be present on Marek's disease tumor cells. It was also unimportant as a target antigen for MDV-related, allogeneic cell-mediated cytotoxicity. The densities of the cells of 5 MDV-induced cell lines were established on continuous Percoll gradients. Most cells had densities between 1.05 and 1.06 g/ml.

Animals↗
PubMed1981

Influence of the bursa of Fabricius on the pathogenesis of Marek's disease.

A series of experiments was conducted to study the influence of embryonal bursectomy (EBX) on the early and late pathogenesis of Marek's disease (MD). The early lytic infection in the lymphoid organs normally associated with oncogenic MD virus infection in intact chickens was not seen in EBX chickens. Therefore, the damage to the immune system was minimal. EBX chickens also had lower viremia levels, higher lymphocyte responses to mitogens, and a lower or delayed MD mortality when compared with intact chickens. Furthermore, it was shown that although vaccination with SB-1 by itself did not protect against a highly virulent MD transplantable tumor, the combination of EBX and vaccination gave significant protection. All these effects could be explained by an enhanced immune response in EBX birds. In contrast, the pathogenesis of nononcogenic MD virus was not influenced by EBX. The possible mechanism(s) involved in these observed effects of EBX on MD pathogenesis are discussed.

Animals↗
PubMed1981

Spontaneous and induced herpesvirus genome expression in Marek's disease tumor cell lines.

We incubated 31 newly established Marek's disease tumor cell lines at 41 degrees C for 48 h after subculturing and then examined them to determine the spontaneous rates of expression of viral internal antigen(s), viral membrane antigen(s), and virus isolation. All but two of the lines were isolated from tumors induced by clone-purified Marek's disease virus strain JM-10, GA-5, RB-1B, and BC-1A in nine different genetic strains of chickens with defined histocompatibility antigens. The line-to-line variations in the rates of spontaneous expression for the antigens or virus rescue were great, but the levels of expression were very low in most cases. The median rates of expression for viral internal antigen, viral membrane antigen, and virus isolation were 32, 8, and 2 positive cells per 10(5) cells, respectively (ranges, 0 to 20,280, 0 to 22,990, and 0 to 220 positive cells per 10(5) cells, respectively). The ratio of viral internal antigen expression to virus isolation was extremely variable and often high, whereas the ratio of viral internal antigen to viral membrane antigen expression was more consistent and generally low. The virus strain which induced the cell line influenced the level of virus genome expression, but the cell genotype did not. Cell lines transformed by JM-10 virus, which exhibited low oncogenicity, had significantly (p less than 0.01) higher rates of expression than cell lines transformed by CA-5 and RB-1B viruses, which exhibited high oncogenicity. Treatment with iododeoxyuridine or incubation at 37 degrees C induced increased rates of expression in most lines but not in all lines. The degree of enhanced expression was inversely proportional to the rate of spontaneous expression.

Animals↗
PubMed1981

Influence of oncogenicity of Marek' disease virus on evaluation of genetic resistance.

Resistance to Marek's disease ( MD) is, in part, genetically determined and linked to the major histocompatability complex. The genetic resistance of 9 previously characterized lines of chickens and also of the inbred UCD-003 and 4 congenic lines was evaluated by challenge with JM-10. Five lines were highly resistant. These included the N-line and two derivatives from N-line (N-2 and N-5), PDRC strain, and one of the congenic UCD lines. The PDRC genotype is unknown, but the 3 related lines carry the B21 allele and the UCD line carries the BQ allele, which appears to be similar to B21. The UCD-003 and the other 3 congenic lines were moderately resistant while S-strain, P-2 and P-5 lines were highly susceptible to JM-10. The total MD incidence varied from 0 to 100% among the lines. Challenge with highly oncogenic virus isolates like GA-5, and especially the recently isolated RB-1B, caused high incidences of MD in all lines and, thus, did not permit differentiation of genetic resistance levels as was possible with the less oncogenic JM-10.

Animals↗
PubMed1981

Latent infections with Marek's disease virus and turkey herpesvirus.

The number of plaque-forming units (PFU) from lymphocytes latently infected with oncogenic (GA-5) or nononcogenic (SB-1) Marek's disease virus (MDV) was decreased after complement lysis with antisera against thymus-derived lymphocytes or bursa-derived lymphocytes; an additive effect with dual treatment was observed. Complement lysis with antisera against Marek's disease tumor-associated surface antigen (putative tumor antigen) had little effect, which suggests an absence of the antigen on latently infected cells. None of the serum complement treatments affected the number of PFU from lymphocytes infected with turkey herpesvirus (HVT). No viral antigens were detected in spleen lymphocytes when removed from infected birds. After 42-72 hours of incubation, many cultured spleen cells from MDV-infected birds (JM-10, GA-5, and SB-1 isolates) contained viral antigen, whereas very few if any cultured cells from HVT-infected birds were positive. These data suggest that the nature of the latent infections with MDV and HVT may differ significantly.

Animals↗
PubMed1980

Inactivated vaccine for parrot herpesvirus infections (Pacheco's disease).

Four tests of an inactivated emulsified vaccine against a herpesvirus infection (Pacheco's disease) in bodgerigars demonstrated that an effective vaccine could be produced with concentrated virus. Virus was propagated in chicken kidney cells, and cells and fluid were harvested 3 to 5 days after inoculation and sonicated. The virus was concentrated 100 x by centrifugation to produce a multiple emulsion vaccine that was protective against IM challenge exposure with live virus. The serologic response after vaccination was negligible, and many survivors to virus challenge exposure did not show a positive titer.

Animals↗
PubMed1979

Demonstration of chicken fetal antigen (CFA) on normal splenic lymphocytes, Marek's disease lymphoblastoid cell lines and other neoplasms.

Chicken fetal antigen (CFA) was detected on normal splenic lymphocytes and a direct relationship was observed between the percentage of CFA-positive cells and the age of the donor. The fetal antigen was also detected on lymphoblastoid tumor cells and cell lines induced by known avian oncogenic viruses (Marek's disease virus and avian leukosis virus), and on spontaneously occurring adenocarcinoma cells. The fetal antigen appears to be distinct from Marek's disease tumor-associated surface antigen.

Adenocarcinoma↗
PubMed1979

In vitro replication of infectious bursal disease virus in established lymphoid cell lines and chicken B lymphocytes.

The in vitro susceptibility of chicken lymphocytes to a wild strains of infectious bursal disease virus was investigated by using immunofluorescence and virus assays as infection criteria. A variety of Marek's disease lymphoblastoid cell lines, all of thymus (T-cell) origin, were refractory to virus exposure. However, a bursa (B-cell)-derived lymphoblastoid cell line from an avian leukosis virus-induced tumor was highly susceptible. Viral antigen appeared in the cytoplasm of 20 to 30% of the cells, and large amounts of cell-free virus were released, with maximum yields occurring by 3 days postinfeciton. The virus also replicated in a small percentage of normal lymphocytes prepared from lymphoid tissues and peripheral blood of chickens. Pretreatment of the lymphocytes, with heat-inactivated anti-B-cell serum or with antiserum against fowl immunoglobulin M before inoculating them with the virus blocked the virus infection; no blocking occurred with anti-T-cell serum or with specific antiserum against fowl immunoglobulin G or immunoglobulin A. This suggests that surface immunoglobulin M-bearing B-lymphocytes were the target cells for infection.

Animals↗
PubMed1979

Pathogenesis of Marek's disease; effect of immunization with inactivated viral and tumor-associated antigens.

Inactivated Marek's disease virus-infected chicken kidney cells and inactivated MSB-1 lymphoblastoid Marek's disease tumor cells were used to immunize chickens as virus- and tumor-associated antigens, respectively. Immune and nonimmune birds were then challenged by exposure to live virulent Marek's disease virus. Both vaccines protected significant numbers of chickens (P less than 0.05) against subsequent tumor development, although viral antigen appeared superior to tumor antigen. After challenge, the early appearance of viral antigen, infected lymphocytes, and degenerative changes in lymphoid organs was inhibited only by the viral antigen vaccine, whereas the early appearance of cells bearing tumor antigen was prevented by both vaccines. These results support the hypothesis that effective immunity in Marek's disease could be directed against either virus replication and spread or events associated with transformation and proliferation of lymphoid cells.

Animals↗
PubMed1979

Comparative pathogenesis studies with oncogenic and nononcogenic Marek's disease viruses and turkey herpesvirus.

An apparently nononcogenic Marek's disease virus (SB-1) and turkey herpesvirus could be readily isolated from spleen, bursa of Fabricius, thymus, and peripheral blood lymphocytes of chickens beginning 4 to 6 days after inoculation, but unlike infections with two isolates of oncogenic Marek's disease virus (JM-10 and CU-2), virus replication in these cells was rare, and necrosis in the organs was essentially absent. Splenic enlargement was observed regularly during the first 4 to 11 days after inoculation, and Marek's disease tumor-associated surface antigen was observed on splenic and other lymphocytes in the four viral inoculation groups. Cellular cytotoxicity of splenic lymphocytes was demonstrated in vitro with cultured Marek's disease tumor cells (MSB-1 lymphoblastoid cell line) as the target in a chromium-release assay. The four viral infections induced sensitized lymphocytes.

Animals↗
PubMed1978

Establishment of Marek's disease lymphoblastoid cell lines from transplantable versus primary lymphomas.

Six new Marek's disease (MD) lymphoblastoid cell lines were established in vitro by cultivation in a medium containing 2-mercaptoethanol (2-ME). Attempts using primary lymphoma cells were generally unsuccessful; only one of 28 lymphomas yielded a cell line and that one came from an experimentally immunosuppressed chicken. In contrast, two of seven low-passage, and two of two established MD transplantable lymphomas grew readily in vitro. A sixth line was obtained using buffy coat cells from a leukemic chicken. It was concluded that the use of transplantable tumor cells and a medium containing 2-ME provided a combination highly suited to the establishment of cell lines from MD.

Animals↗
PubMed1978

Characterization of an apparently nononcogenic Marek's disease virus.

A new isolate of Marek's disease virus (MDV) was described. This virus, SB, and a clone, SB-1, differed from pathogenic isolates in in vitro growth characteristics as described for other apathogenic isolates. Serologically, as with other apathogenic isolates, SB could be distinguished from pathogenic MDV and the avirulent turkey herpesvirus. SB failed to induce lesions characteristic of Marek's disease (MD) during a 6- to 11-week experimental period. Also, SB was nononcogenic in immunosuppressed chickens or in chickens inoculated with this virus in ovo. However, under those conditions, SB caused a cytolytic infection. The term "nononcogenic" rather than "apopathogenic" was therefore proposed to classify this and similar isolates. SB-1 protected chickens against challenge with either virulent MDV or the non-virus-producing MD tumor transplant, JMV. Possible mechanisms of protection are discussed.

Animals↗
PubMed1978

Protection against Marek's disease-derived tumor transplants by the nononcogenic SB-1 strain of Marek's disease virus.

A series of experiments was conducted to study the in vivo protection against Marek's disease-derived tumor transplants by the nononcogenic SB-1 strain of Marek's disease virus. Intact, embryonally bursectomized (Bx), thymectomized (Tx), or cyclophosphamide (Cy)-treated chickens of four genetic lines were vaccinated with live or inactivated SB-1. JMV, a non-virus-producing transplant, and GA/Tr-1 and MDT-198, two virus-producing transplants were used for challenge. Optimal protection against JMV was present 7 days postvaccination, but there was significant protection even when SB-1 and JMV were administered together. Protection was abolished by an increase in the number of tumor cells used for challenge or by combined Tx and Cy treatment. Inactivated SB-1-infected cells were unable to induce protection against JMV challenge. Protection was also present against challenge with GA/Tr-1, but not against MDT-198, except in vaccinated, Bx chickens. It was concluded that protection against JMV was T-cell dependent and required the induction of neo-antigens not present in an inactivated SB-1 cellular preparation. The absence of protection in intact chickens against MDT-198 could not be explained.

Animals↗