Bovine adenovirus type 3 (BAV3) was purified and its properties were studied. On productive infection of CKT1 cells (a cell line derived from calf kidney) with BAV3, it was observed that viral DNA synthesis was initiated after about 24 h and its rate was maximal after about 40 h. Maturation of the virus occurred several hours after this. Purified BAV3 was separated into four discrete bands by CsCl density gradient centrifugation (complete, incomplete, empty, and degraded viruses). The complete BAV3 was similar in size and structure to human and avian adenoviruses. Polyacrylamide gel electrophoresis showed that the complete BAV3 virion contained at least 10 polypeptides. The total structural proteins of the virion had a similar amino acid composition to those of human adenoviruses. DNA of the complete virus was a linear duplex and its contour length was 12.3 4 0.9 um. The S' value of the DNA was 32.9S and its buoyant density in CsCl was 1.717 g/ml. There was about 25% homology between the DNAs of BAV3 and human adenovirus type 5 by filter hybridization. It was also noted that BAV3 produced incomplete virus. The incomplete virus was similar in morphology to the complete virus and contained almost all the structural polypeptides of the latter, but lacked infectivity. However, its DNA had a deletion(s) (13%) which seemed to locate near a terminal.
Hepatic fibrosis was induced in rats by repeated i.p. injections of pig serum. The hepatic hydroxyproline content increased to 2.1 times the normal control level at 6 weeks and to 3.2 times at 10 weeks. When P-1894B, an inhibitor of prolyl hydroxylase, was administered, there was a dose-dependent inhibition of the increase to nearly normal control levels at 6 and 10 weeks. There was also by histology a dose-dependent reduction in the degree of hepatic fibrosis. Hepatocellular damage was minimal and its extent did not vary with the degree of fibrosis or the treatment. P-1894B dose dependently reduced the hydroxylation of peptidyl proline in the fibrotic liver. These data suggest that P-1894B inhibited hepatic fibrogenesis by direct action on collagen but not by protection against hepatocellular damage leading to collagen formation. A prolyl hydroxylase inhibitor may be a candidate for use in treatment of hepatic fibrosis.
Incomplete virus of oncogenic bovine adenovirus type 3 (BAV3) was highly purified and its biological activity was studied. The production of incomplete virus was found to increase with a high multiplicity of infection and with a large amount of arginine in the growth medium. On infection of contact-inhibited mouse cells, incomplete virus induced cellular DNA synthesis and focus formation. Moreover, this virus was oncogenic to newborn hamsters. On infection of calf kidney cells, a permissive cell line, viral early and late RNA, viral DNA, and almost all the viral late proteins were produced, but no mature progeny virus was detected. It is, therefore, suggested that incomplete virus of BAV3 may be unable to synthesize a protein(s) (perhaps a kind of maturation protein [s]) essential for
ABSTRACT. Some properties of A31 cells (a clonal line of BALB/3T3 cells) transformed by fragments of DNA of bovine adenovirus type 3 (BAV3), i.e., EcoRI D fragments (3.6 to 19.7 map units of viral genome) or HindIII J-E ligated fragments (0 to 11.9 map units) produced by restriction endonuclease digestion, were examined. These transformed cells were found to commonly contain most, if not all, of the nucleotide sequences in the region of from 3.6 to 11.9 map units of BAV3 genome, by DNA-DNA reassociation kinetics analysis. Moreover, the synthesis of virus-specific RNA was detected by DNA-RNA hybridization experiments. TrD and TrJE cells (A31 cells transformed with Eco RI D fragments and HindIII J-E ligated fragments of BAV3 DNA, respectively) as well as A31 cells transformed with whole viral DNA or BAV3, showed a rapid uptake of 2-deoxyglucose, high cell agglutinability by plant lectins and high plasminogen acivator activity, in comparison with A31 cells. All these transformed cells produced tumors when inoculated subcutaneously into adult BALB/c mice. These results indicated that all these characteristics examined are directly or indirectly controlled by the gene(s) located between the map units of 3.6 and 11.9 of the BAV3 genome.The analyses of viral DNA seauences present in cells transformed by human adenoviruses have revealed that the transforming gene(s) of human adenoviruses are located at the left hand end of the viral genome (9, 26, 28, 32). Moreover, investigations of the transformation of cells with DNA fragments of human adenoviruses have determined the locus of the gene(s) more precisely (9, 26, 28, 32), and some properties of the resulting transformed cells have been examined (28, 32).In the preceeding paper, we reported the physical maps of bovine adenovirus type 3 (BAV3) DNA using the restriction endonucleases EcoRI, BamHI and HindIII (16). We also demonstrated that the transformation of mouse A31 cells could be induced by BAV3 DNA EcoRI D fragments and ligated DNA of HindIII J and E fragments (12). And it was concluded that the transforming gene(s) of BAV3 were located in the region between 3.6 and 11.9 map units of the viral genome. A31 cell lines, trans-
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