Zz. Xu et al., An ovine adenovirus vector lacks transforming ability in cells that are transformed by AD5 E1A/B sequences, VIROLOGY, 270(1), 2000, pp. 162-172
Adenoviruses of the Mastadenovirus and Aviadenovirus genera are able to tra
nsform certain cell types and induce tumor formation in susceptible animals
. For the mastadenoviruses the E1A/B sequences are largely responsible for
these properties but E4 sequences may also be involved. The transforming se
quences of the aviadenoviruses, which lack E1A/B and E4 homologues, have no
t yet been fully identified. The recent proposal for a third genus of adeno
viruses, which apparently lack an EIA homologue and have weak E1B homology,
prompted an examination of the transforming properties of ovine adenovirus
OAV287 (OAV), the prototype member of the new group. When OAV and human ad
enovirus type 5 (Ad5) were used to infect primary rat embryo cells, transfo
rmed foci developed in Ad5- but not in OAV-infected cultures. Similarly, af
ter plasmid transfection, baby rat kidney cells were transformed by Ad5 E1A
/B but not by OAV sequences. When CSL503 cells, an ovine cell line that is
permissive for OAV, were transfected with Ad5 E1A/B sequences, transformed
foci again appeared. However, plasmids or fragments containing complete or
partial OAV genome sequences did not detectably transform CSL503 cells unde
r the same conditions. When Ad5 E1A/B sequences were incorporated into the
complete OAV genome and transfected, transformed clones were again obtained
, showing that the gene dosage and transfection conditions were not limitin
g for transformation. The provision of Ad5 E1A and OAV sequences in combina
tion marginally increased the number of morphologically altered foci in bab
y rat kidney cells but failed to induce multilayered focus formation. The d
ata suggest that OAV lacks transforming functions in the cell types examine
d. Additional information suggesting that OAV may have a fundamentally dist
inct strategy for replication compared with other Ads is discussed. (C) 200
0 Academic Press.