Cumulative author index for volumes 132–139

Abstract

The functional relatedness of the transforming genes (E1a and E1b) of adenovirus type 9 (group D) which induces mammary tumors in rats and those of the non-tumorigenic adenoviruses, Ad2 and Ad5 (group C) was examined. Transfection of established rat embryo cells with a DNA segment containing the E1a and E1b regions of Ad9 resulted in efficient transformation; similar results have been shown for group A, B and C Ads. In contrast to Ads of group A, B and C, Ad9 DNA containing the E1 region or the entire viral genome was unable to transform primary baby rat kidney (BRK) cells. The functional relatedness of genes encoded within the E1 region was compared using a mutant complementation assay in which various group C mutants defective in the entire E1 region or in the E1a or E1b regions alone as well as mutants defective exclusively within the 19K or 58K T antigens coding regions of Elb were coinfected with wild type (wt) Ad9 and tested for group C mutant DNA replication, virus production, or expression of early and late genes. These studies have shown that a defect in the entire E1 region of Ad2 could only be complemented poorly by Ad9; our earlier studies have shown that coinfection with Ad12 (group A) or Ad7 (group B) resulted in efficient complementation (Brusca and Chinnadurai (1981) J. Virol. 39, 300–305). Further analysis indicated that a defect in the E1a region could be complemented by the group D E1a region. The level of E1a complementation as judged by mutant DNA replication and activation of expression of mutant early viral genes was about one-fourth to one-fifth the level in 293 cells that constitutively express Ad5 E1a and E1b regions. Our results indicate that a defect in the E1b 19K T antigen, which leads to degradation of intracellular DNA in infected cells, could be complemented by the group D protein. However, a defect in the E1b 58K T antigen could not be efficiently complemented by the group D protein. Coinfection of group C mutants defective in the 58K T antigen and Ad9 wt did not lead to an increase in the mutant viral production. Furthermore, in cells coinfected with the 58K T antigen mutants and Ad9 wt there was a large reduction in the accumulation of group C late cytoplasmic RNA. The observed complementation defect of Ad9 in supporting multiplication of group C mutants defective in the entire E1 region may therefore be a cumulative effect of both E1a and E1b regions.