TY - JOUR
T1 - Suppression of the temperature-sensitive character of adenovirus 12 early mutants in monkey cells transformed by an adenovirus 7-simian virus 40 hybrid
AU - Shiroki, Kazuko
AU - Shimojo, Hiroto
AU - Sekikawa, Kenji
AU - Fujinaga, Kei
AU - Rabek, Jeffrey
AU - Levine, Arnold J.
N1 - Funding Information:
and from the Mitsubishi Foundation and by the American Cancer Society, Grant No. E 591.
Funding Information:
ACKNOWLEDGMENTS This work was supported in part by grants from Ministry of Education, Science and Culture of Japan
PY - 1976/2
Y1 - 1976/2
N2 - Temperature-sensitive mutants of adenovirus 12, defective in viral DNA replication, fall into three complementation groups; tsA, tsB and tsC. Each of these classes was temperature dependent for virus production, viral DNA synthesis and virion antigen in human embryonic kidney cells and in T22 cells, a monkey cell line transformed by defective particles of simian virus 40 (SV40). In H5 cells, a monkey cell line transformed by an adenovirus 7-SV40 hybrid, however, the tsB and tsC mutants were not temperature sensitive for viral replication while the tsA mutant retained its temperature-sensitive phenotype. Wild-type adenovirus 7, but not wild-type SV40, was able to complement tsA, tsB and tsC for either infectious virus production or DNA replication. These observations suggest that adenovirus 7-specific functions present in the H5 cells complement or suppress the tsB and tsC gene functions. DNA-DNA reassociation kinetics and DNA-RNA hybridization competition experiments have been performed and demonstrate the presence and the transcription of at least a portion of the adenovirus 7 genome in the H5 cells.
AB - Temperature-sensitive mutants of adenovirus 12, defective in viral DNA replication, fall into three complementation groups; tsA, tsB and tsC. Each of these classes was temperature dependent for virus production, viral DNA synthesis and virion antigen in human embryonic kidney cells and in T22 cells, a monkey cell line transformed by defective particles of simian virus 40 (SV40). In H5 cells, a monkey cell line transformed by an adenovirus 7-SV40 hybrid, however, the tsB and tsC mutants were not temperature sensitive for viral replication while the tsA mutant retained its temperature-sensitive phenotype. Wild-type adenovirus 7, but not wild-type SV40, was able to complement tsA, tsB and tsC for either infectious virus production or DNA replication. These observations suggest that adenovirus 7-specific functions present in the H5 cells complement or suppress the tsB and tsC gene functions. DNA-DNA reassociation kinetics and DNA-RNA hybridization competition experiments have been performed and demonstrate the presence and the transcription of at least a portion of the adenovirus 7 genome in the H5 cells.
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U2 - 10.1016/0042-6822(76)90474-8
DO - 10.1016/0042-6822(76)90474-8
M3 - Article
C2 - 176780
AN - SCOPUS:0017283461
SN - 0042-6822
VL - 69
SP - 431
EP - 437
JO - Virology
JF - Virology
IS - 2
ER -