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Biomedical subjects

J W Beard

Publications and source records attributed to J W Beard.

10 recordsLinked to original sources
PubMed1979

Reverse transcriptase from avian myeloblastosis virus.

From lots of 20 to 30 g of avian myeloblastosis virus RNA-dependent DNA polymerase was obtained in preparations of purity greater than 95% by using a two-step column chromatographic procedure employing DEAE (DE 52) and carboxymethylcellulose (CM 52.). Yields of RNA-dependent DNA polymerase varied from approximately 20,000 to 35,000 U/g of virus. Specific activity of the enzyme was about 35,000 to 60,000 U/mg of protein. Free of detectable RNase activity, the product exhibited a molecular weight of about 160,000, an isoelectric point of 6.5, and approximately 2 mol of fatty acid per mol of enzyme.

Animals↗
PubMed1978

Protein kinase from avian myeloblastosis virus.

A protein kinase associated with purified virions of avian myeloblastosis BAI strain A was partially purified by ion-exchange chromatography and gel filtration. The transfer of phosphate catalyzed by this enzyme required a divalent metal ion and ATP as phosphate donor. GTP could not be substituted for ATP, and the reaction was unaffected by either cyclic AMP or beef-heart protein-kinase inhibitor. Of the virus and nonvirus proteins tested as phosphate acceptors, only acidic proteins were phosphorylated. In particular, purified preparations of reverse transcriptase from avian myeloblastosis virus did not accept phosphate. The enzyme is a basic protein (pI = 9.3), and, on the basis of molecular sieving through Sephadex G-200 and velocity sedimentation on glycerol gradient, the protein kinase has a molecular weight of 45,000.

Adenosine Triphosphate↗
PubMed1976

Influence of phosphate on activity and stability of reverse transcriptase from avian myeloblastosis virus.

Activity of RNA-dependent DNA polymerase (RDDP) from avian myeloblastosis virus (AMV), either in purified form or in virus lysates, was increased by phosphorylation. Stability of RDDP in lysates buffered with phosphate was much greater (no loss of activity in 48 hours at 4 degrees) than that in lysates buffered with Tris-Cl (76% loss). Activity lost in the Tris-buffered extracts was completely restored by phosphorylation. The findings suggested that AMV RDDP activity is influenced by the degree of phosphorylation of the enzyme or enzyme-associated proteins and that this chemical modification is mediated by protein phosphokinase and phosphoprotein phosphatase present in crude extracts of purified AMV. Application of these results provided the basis of procedures whereby RDDP can be recovered in significantly higher yield and purity than formerly.

Adenosine Triphosphate↗
PubMed1976

Renal neoplastic response to leukosis virus strains BAI A (avian myeloblastosis virus) and MC29.

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.

Adenocarcinoma↗
PubMed1976

Virus-infected avian cell lines established in vitro.

Four virus-infected avian cell lines have been established in culture. Two of these lines, infected with BAI strain A virus, liberate only small quantities of virus in the culture fluid. The cells retain the ability to induce myeloblastic leukemia when inoculated i.v. into 1- to 2-day-old chicks, but do so less efficiently than freshly obtained myeloblasts. These cells do not appear to be transplantable, since the disease produced is characterized by the presence of myeloblasts that liberate large quantities of virus. The other two cell lines, infected with the MC29 strain of avian leukosis virus, liberate normal levels of infectious virus in the culture fluid. When these cells are inoculated into the wing web of 1- to 2-day-old chicks, tumors develop at the site of inoculation which are detectable as early as 4 to 7 days after challenge. Chromosome studies demonstrate that the four cell lines have karyotypes typical of Gallus domesticus. The myeloblastic cell lines (D.U. 11157 and D.U. 1765) show a reduction in the number of microchromosomes. These cell lines have been carried in continuous culture for various lengths of time, can be frozen, are easily recovered in viable form, and appear to be capable of indefinite growth.

Adenosine Triphosphatases↗
PubMed1975

Transplantation of hepatomas induced in the avian liver by MC29 leukosis virus.

A hepatomatous growth derived from primary liver tumors induced in chickens by i.v. inoculation with MC29 leukosis virus has been established and maintained in the avian host. Hepatoma tissue transplanted into the abdominal cavity in a total of 278 chicks in 35 experiments yielded tumors in 222 animals (80%). The i.m. implantation in 69 birds in 7 experiments resulted in growth in 67 chicks (97%). Tumor tissue introduced inadvertently into the s.c. tissue likewise grew very rapidly. Histological and cytological features of the transplants in all sites showed preservation of the morphological characteristics of the original primary liver tumors through repeated passages. The properties of this first transplantable hepatoma derived from virus-induced primary liver tumors are compared with those of other transplantable hepatomas.

Abdomen↗
PubMed1975

Neoplastic response of the avian liver to host infection with strain Mc29 leukosis verus.

Studies were made on the oncogenic response of 3086 young chicks to i.v. inoculation of MC29 avian leukosis virus from blood plasma of previous-passage birds or the supernatant fluid of cultures of chick embryo cells infected with strain MC29. Among the large variety of neoplasms of other tissues previously described, there occurred a high incidence of primary growths of the liver. Pathomorphology of the growths frequently differed greatly in both different hosts and the same bird, but some uniformity of the types of neoplasms was evident in many animals. Despite much variation in histopathology, the large proportion of growths could be grouped in several distinctive categories. Examinations by light and electron microscopy provided evidence of derivation of the tumors by alteration of hepatocytes originating principally in the portal regions as indicated by forms transitional from the parenchymal cells to the cells of the different types of growths. Neoplastic aspects of the growths were evident by infiltration and invasion of adjacent tissues, penetration of blood vessels, transplantability to other avian hosts (described in another report), and metastasis to distant organs including the lung, kidney, and spleen. There was no evidence of tumors arising from the biliary system, and growths of cells resembling the biliary type could be traced to altered hepatocytes. None of the findings suggested conversion of biliary-type cells to hepatocytes. Continued growth resulted in anaplastic and metaplastic changes in cell morphology and structural organization and in the formation of cartilage, osteoid, and sarcoma-like spindle-cell tumors of probable epithelial origin. Development of the growths wasnot associated with cirrhosis, and necrosis was limited to infrequent disseminated, essentially unicellular changes or necrobiosis of small groups of cells. The marked variations in the type of virus-induced growths demonstrated the remarkable capacity of cells morphologically inidistinguishable from the hepatocytes for the most diverse alterations in cell structure and tissue organization. This neoplastic response of hepatocytes to the MC29 strain constitutes the only demonstration thus far of the specific hepatocarcinogenic activity of an avian tumor virus.

Adenocarcinoma↗
PubMed1971

Component of strain MC29 avian leukosis virus with the property of defectiveness.

Three clones of morphologically altered cells (L(-)MC29) of singular properties were isolated from MC29 (subgroup A) leukosis virus-infected chick embryo cells. Supernatant fluids from cultures of the cloned cells produced no transforming or interfering activity on chick embryo cells susceptible to known avian leukosis-sarcoma viruses. No virus associated with the cells was demonstrable by fluorescent-antibody staining or by electron microscopy. All L(-)MC29 clone cells were activated, however, by four strains of Rous-associated viruses (RAV) representative of A, B, C, and D subgroup avian leukosis viruses and by two strains of MC29 virus. Virus L(-)MC29 cells activated by superinfection with RAV-1 and RAV-2 was characterized by helper-dependent and helper-independent properties. These findings suggest that the strain MC29 leukosis virus, or a component thereof, possesses properties of defectiveness similar to those of the Bryan high-titer Rous sarcoma virus.

Animals↗