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Query: UMLS:C0679427 (myeloblastosis)
 982 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous reports described the induction of avian renal neoplasms by leukosis virus strains BAI A [avian myeloblastosis virus (AMV)] and MC29, and illustrated morphological characteristics of the tumors. Continued studies in this work confirm evidence of the origin of the tumors from embryonal cells residual in the posthatched chick. The work further emphasizes differences in histopathology of the neoplasms caused by the two viruses and reveals differences in the histopathogenesis of the respective growths. Embryonal rests may consist of two types of cells, those of epithelial characteristics and a second element of differentiation between nephroblastema (mesenchyme) and epithelium and designated here as nephromesoblastoma. Infection by AMV induces tumors of epithelial characteristics and, in addition, derivatives of nephromesoblastoma consisting of cartilage, bone, areas of keratinization, and sarcoma. Keratinized structures in the nephroblastoma originate from nephromesoblastoma. In contrast, MC29 virus induces only epithelial growths representing principally aberrant and malformed glomerular and tubular structures with occasional cartilage derived from epithelial cells. MC29 tumors are completely lacking in nephromesoblastoma tissue and contain no bone, sarcoma, or keratinized formations. In MC29 tumors, occasional cartilage was derived from epithelium. Tumors caused by AMV exhibit the complex structure of nephroblastoma with all of the features of the growth in humans (Wilms' tumor). The neoplasms induced by both AMV and MC29 exhibit marked aberration, distortion, and malformation in the differentiation of the cells growing out from the embryonal rests representing rare manifestations of cell genetic influence inherent in the primordial growth of nephroblastema. The results thus illustrate fundamental differences in cellular composition and capacity to respond to etiologically different leukosis viruses.
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PMID:Renal neoplastic response to leukosis virus strains BAI A (avian myeloblastosis virus) and MC29. 17 94

Infection of chickens with a myeloblastosis-associated virus which induced a high incidence of osteopetrosis was accompanied by immunosuppression. The immunosuppression was manifested in the following ways. The weight of the bursa, spleen, and thymus was depressed in infected chickens. Infected animals had a diminished capacity to form hemolytic plaques in a direct assay. Spleen cells from osteopetrotic animals did not respond to phytohemagglutinin, and the spleen and bursa had a decreased proportion of cells possessing surface immunoglobulin. Osteopetrotic animals failed to show an age-dependent increase in the proportion of cells demonstrating surface immunoglobulin that was observed in normal animals. However, several individual chickens with heavy osteopetrosis responded to antigenic stimulation in a normal fashion, indicating that although immunosuppression usually accompanies avian osteopetrosis, it may not contribute directly to abnormal bone proliferation.
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PMID:Characterization of the immunosuppression accompanying virus-induced avian osteopetrosis. 73 Mar 67

Infection of 10-day-old chickens with an avian osteopetrosis virus resulted in a severe regenerative aplastic crisis. Hematopoietic and lymphopoietic tissues of chickens infected with myeloblastosis-associated virus (of subgroup B, inducing osteopetrosis, MAV-2(O] were analyzed for integrated and unintegrated viral DNA sequences, cell population shifts, weight changes, and morphological alterations. By 6 days postinfection (p.i.), DNA from bone marrow cells and peripheral blood leukocytes (PBL) contained between 0.50 and 0.70 copies of viral DNA per haploid genome. Erythrocytes and splenic leukocytes contained less than 0.10 copies/haploid genome. Granulocytes and precursor mesomyelocytes were absent from bone marrow, but numbers of erythrocytes, erythroblasts, and reticulocytes were normal. By 9 days p.i., bone marrow was severely hypoplastic and both granulopoietic and erythropoietic colonies were depleted. By 12 days p.i., erythrocytes and granulocytes were maximally depressed in peripheral blood and the amount of integrated virus in bone marrow and PBL decreased to less than 0.20 copies/haploid genome. In contrast, erythrocytes contained integrated viral DNA of up to 0.30 copies/haploid genome, indicating infection of erythrocyte precursors. At 18 days p.i., viral DNA was detected only in erythrocytes. Unintegrated viral DNA was not detected in any organs. Anemia was accompanied by splenomegaly and erythrophagocytosis. Viral DNA was never detected in thymus or bursa. Differential counting and flow cytometry of cells from bursa, thymus, and spleen, and of blood lymphocytes did not detect significant population shifts. These results suggest that MAV-2(O) infection of immunocompetent chickens occurs primarily in myelopoietic tissues, and tissues are selectively infected.
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PMID:Analysis of hematopoietic and lymphopoietic tissue during a regenerative aplastic crisis induced by avian retrovirus MAV-2(O). 283 18

The cupric and ferric complexes of isonicotinic acid hydrazide (INH) inhibit the DNA synthesis catalysed by avian myeloblastosis virus (AMV) reverse transcriptase. The inhibition was to the extent of 95% by 50 microM of cupric-INH complex and 55% by 100 microM of ferric-INH complex. These complexes have been found to bind preferentially to the enzyme than to the template-primer. Kinetic analysis showed that the cupric-INH complex is a non-competitive inhibitor with respect to dTTP. The time course of inhibition has revealed that the complexes are inhibitory even after the initiation of polynucleotide synthesis. In vivo toxicity studies in 1-day-old chicks have shown that the complexes are not toxic up to a concentration of 500 microgram per chick. Infection of the 1-day-old chicks with AMV pretreated with 150 microgram of either of the complexes prevented symptoms of leukemia due to virus inactivation.
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PMID:Inhibition of avian myeloblastosis virus reverse transcriptase and virus inactivation by metal complexes of isonicotinic acid hydrazide. 618 90

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.
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PMID:Inhibition of concanavalin A response during osteopetrosis virus infection. 621 95

Infection of cultured stage 24 (day 4.5) chick limb cells (spot cultures) with myeloblastosis-associated virus 2-(osteo) (MAV-2(0)) produces cell density-dependent alterations of collagen and noncollagen protein synthesis over the course of 8 days in culture. Collagen synthesis in infected, low density cultures (100 k cells/spot) was maximal on day 4 and increased 12 fold compared with maximal values on days 5-6 for uninfected counterparts. The patterns of collagen synthesis were similar in uninfected or MAV-2(0)-infected cultures seeded at 200 (medium density) or 400 k cells (high density) per spot with peaks on days 5-6. Noncollagen protein synthesis (NCP) in infected, low density cultures was maximal on day 4 and increased 15.7 fold compared with maximal values on days 5-6 for uninfected counterparts. The patterns for NCP synthesis were similar for uninfected and MAV-2(0)-infected cultures seeded at medium density (peak on day 5). However, in MAV-2(0)-infected , high density cultures, NCP synthesis was maximal on day 4 and increased 2.9 fold compared with maximal values on days 5-6 for uninfected counterparts. Although kinetics of cell division and DNA synthesis were similar in uninfected and MAV-2(0)-infected limb bud cells, the virus may have diverse affects on different cell populations at the three cell densities employed in these experiments.
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PMID:Collagen and noncollagen protein synthesis in chick limb bud cells infected with a virus that causes osteoblastoma. 728 76