concanavalin-a and Avian-Leukosis

Studies were performed to determine the effects of Bcell suppression on the pathogenesis of Subgroup J avian leukosis virus (ALV-J) in broiler chickens. Neonatal chickens were treated with cyclophosphamide (CY) or PBS, and then infected with ALV-J (ADOL-7501) at 2 weeks of age. CY treatment induced B cell specific immunosuppression throughout the experiment confirmed by decreased bursal weight, intact lymphocyte mitogenetic activity stimulated by Con A and increased relative subpopulation of CD3-positive cells as measured by flow cytometry. Chickens in this experiment had Mareks disease virus exposure prior to three weeks of age as determined by the presence of lymphocytic infiltration and antibody. Virus neutralizing antibody against ALV-J was first observed at 6 weeks post-infection in some of the infected chickens in the PBS group. As expected, none of the chickens from the CY group and uninfected chickens developed virus-neutralizing antibody. The viremic status was measured by real time RT-PCR using SYBR green I dye. The percentage of viremic chickens was significantly higher, and more chickens had high titered viremia, in the CY treated group. No neoplastic foci consistent with ALVJ infection were observed in any of the experimental chickens. The frequency and intensity of viral antigen expression determined by immunohistochemistry was significantly higher in tissues from CY treated birds than those of PBS treated chickens at 3 weeks post-infection. This study showed that B cell specific immunosuppression with CY treatment in chickens resulted in increase in viremia and viral antigen load in tissues.

Topics: Animals; Avian Leukosis; Avian Leukosis Virus; Benzothiazoles; Body Weight; Bursa of Fabricius; Chickens; Concanavalin A; Cyclophosphamide; Diamines; Flow Cytometry; Immunocompromised Host; Immunohistochemistry; Immunophenotyping; Immunosuppressive Agents; Lymphocyte Activation; Organic Chemicals; Poultry Diseases; Quinolines; Random Allocation; Reverse Transcriptase Polymerase Chain Reaction; RNA, Viral; Spleen; Statistics, Nonparametric; Viremia

Infection of chicks or chick embryos with Rous associated virus number 7 (RAV-7) led to a decreased blastogenic response to Concanavalin A (Con A) by lymphocytes isolated from the spleen and thymus. Chicks infected with RAV-7 8 days after hatch manifested decreased Con A blastogenesis 5 weeks postinfection, while chicks infected in ovo at 10 days of incubation showed an unusual pattern of cell density dependent decreased blastogenesis two weeks post-hatch (three weeks post-infection). Histopathological examination of tissues from RAV-7 infected chicks revealed evidence of lymphoid organ involution and widespread lymphoproliferative lesions by 3 weeks of age. The combination of decreased in vitro lymphoid blastogenesis and in vivo lymphoproliferation suggests that RAV-7 interacts with lymphocytes in a fashion that has not previously been described in the chicken.

Topics: Animals; Avian Leukosis; Avian Leukosis Virus; Bone Marrow; Chick Embryo; Chickens; Concanavalin A; Lymphocyte Activation; Lymphocytes; Myocardium; Spleen; T-Lymphocytes; Thymus Gland

Infection of animals with oncogenic viruses frequently leads to an immunosuppressed state. We have examined immunosuppression induced by an avian osteopetrosis virus, myeloblastosis-associated virus of subgroup B inducing osteopetrosis [MAV-2(O)], and our results suggest that this virus induces immunosuppression by a novel mechanism. Lymphoid cells from osteopetrotic chickens did not respond to a wide dose range of concanavalin A (Con A) over a wide cell density range. Failure to undergo blastogenesis was not due to a lack of Con A-binding sites, since 125I-labeled Con A bound to lymphocytes from infected and uninfected chickens. Infected lymphocytes failed to respond to sodium metaperiodate stimulation, indicating that failure of blastogenesis was not due to a blockage of Con A receptor sites. MAV-2(O) infection of chicks 8 days of age resulted in a transient immunosuppression which appeared 1 to 2 weeks after infection. Cell-mixing experiments showed that MAV-2(O)-induced immunosuppression was not attributable to suppressor cells. In contrast, adherent cells from normal lymphoid preparations restored mitogenicity to lymphocytes from MAV-2(O)-infected animals. Adherent cells were present in the spleen and peripheral blood lymphocytes of MAV-2(O)-infected chickens in numbers comparable to those of the uninfected animal, and both sets of cells contained Fc-dependent phagocytic activity and nonspecific esterase. Peritoneal exudate cells were elicited from osteopetrotic and normal chickens in similar numbers. We conclude that MAV-2(O) induces immunosuppression by interfering with an accessory function of macrophage-like adherent cells.

Topics: Anemia; Animals; Avian Leukosis; Avian Myeloblastosis Virus; Chickens; Concanavalin A; Immune Tolerance; Lymphocyte Activation; Macrophages; Osteopetrosis; Receptors, Concanavalin A; Satellite Viruses; T-Lymphocytes, Regulatory