The oncogenicity of avian adenoviruses I. An unusually large number of viral DNA molecules in some tumors, and virus-specific T-antigenic proteins

DNA-binding Proteins of Chick Embryo Lethal Orphan Virus: Lack of Complementation between Early Proteins of Avian and Human Adenoviruses

“…BHK cells werc found to express CELO virus DNA-binding proteins, and hamster cells also cxpress CELO virus T antigens (Asch et aL, 1979;Ishibashi et aL, 1980), but co-infection of BHK cells with CELO virus and Ad5 early gene mutants suggested that there was no complementation by CELO virus early proteins of Ad5 early functions carried out by Ad5 E 1A proteins, Ad5-encoded 140K DNA polymerase or Ad5 72K DNA-binding protein. Our data do not exclude complementation in the other direction; however, this seems unlikely due to the failure of CELO virus to produce DNA-binding protein in 293 cells.…”

“…To investigate further the possible functional links between human and avian adenoviruses, the ability of CELO virus early gene products to complement mutant human adenovirus early functions in BHK cells was tested. Hamster BHK cells are permissive to subgroup C human adenoviruses, and allow synthesis of CELO virus DNA-binding proteins: they also produce CELO virus tumour-specific (T) antigens (Asch et al, 1979: Ishibashi et al, 1980. Confluent BHK cells were mock-infected or infected with CELO virus at 50 i.u./cell, or infected with Ad5 at 25 i.u./cell, or co-infected with 50 i.u./cell of CELO virus and 25 i.u./cell of one of the following Ad5 early mutants: dl312, a deletion mutant that lacks the promoter and most of the coding sequence of the E 1A region ; d1314, a deletion mutant that lacks most of the 3' exon of E1A ; ts36, a temperature-sensitive mutant which carries lesion(s) in gene N in the E2B region of the Ad5 genome that encodes the 140K viral DNA polymerase (Williams et al, 1974;Galos et al, 1979: Stillman et al, 1982: and ts125, a temperature-sensitive mutant which carries a mutation in the gene coding for the 72K DBP (van der Vliet et al, 1975).…”

“…Yasue & Ishibashi (1977) reported eight chick embryo lethal orphan (CELO) virus-induced early polypeptides that could be detected in infected cells in the presence of cytosine arabinoside. Asch et al (1979) and Ishibashi et al (1980) described CELO virus tumour (T) antigens that reacted with sera from animals bearing CELO virus-induced tumours, and were also produced in infected cells in the presence of cytosine arabinoside. It is likely that CELO virus codes for one or more DNAbinding proteins (DBP), since CELO virus DNA replication shares general similarities with that of human adenovirus, and CELO virus DNA replication intermediates have extensive single-stranded regions (Bellett & Younghusband, 1972).…”

Preferential clustering of viral DNA sequences at or near the site of chromosomal rearrangement in fowl adenovirus type 1 DNA-transformed cell lines

“…Tumorigenicity in rodents (15) and transforming activity in cultured cells (1) were found for FAV-1 soon after these findings were obtained for human adenoviruses. As a part of our studies on the oncogenicity of FAV-1, we induced tumors in rodents by subcutaneous inoculation of the virus and analyzed the molecular arrangement of viral DNA sequences in several lines of the tumors by Southern blot hybridization (11,22,23) and the chromosomal arrangement in one of these tumors by in situ DNA hybridization (22). We inferred from these experiments that in many tumor lines, viral DNA sequences together with flanking cellular DNA sequences were reiterated more than a hundredfold and clustered at limited sites on marker chromosomes.…”

Grouping of Fowl Adenoviruses Based upon the

“…Based on their immuno logical properties, 41 serotypes have been distinguished [1], and these have been grouped according to their hemagglutinating ability [2], oncogenicity [3], polypeptide structure [4], and genome composition [5,6], On the other hand, the fowl adenoviruses have been distinguished primarily on the ba sis of their immunological properties. Ac-cording to the most recent results, there are 11 serotypes of fowl adenoviruses [7], Al though experiments have been done to group them on the basis of other criteria, e.g., on cogenicity [8] and intranuclear inclusion body formation [9], either too few virus strains were included or the criterion chosen was not adequate. Therefore, we have at tempted to classify the fowl adenovirus strains described thus far and to group them on the basis of a property which is indicative of their genome structure.…”