E1B functions of type C adenoviruses play a role in the complementation of blocked adenovirus type 12 DNA replication and late gene transcription in hamster cells.

Adenovirus type 12 (Ad12) DNA cannot replicate in hamster cells and the late Ad12 genes cannot be expressed. It has been demonstrated previously that these defects can be at least partly overcome by coinfection of hamster cells with Ad12 and wild-type adenovirus type 2 (Ad2) or type 5 (Ad5) or by superinfection of Ad2- or Ad5-transformed cells with Ad12. These transformed cell lines carry in an integrated form and constitutively express the E1 region of Ad2 or Ad5. The compensation in Ad12 DNA replication and late gene transcription does not, however, lead to the assembly of intact Ad12 virions. In the present study, it has been demonstrated that the complementing functions in the Ad5 genome, which can effect Ad12 DNA replication and late transcription in hamster cells, reside predominantly but not exclusively in the E1B region. A supporting role in the E1A region is likely. These conclusions have been adduced from the results of double infection experiments using Ad12 and deletion mutants of Ad5. Inside the E1B region of Ad5 DNA, the complementing functions have not yet been precisely located. Although late Ad12 messenger RNAs are synthesized in Ad12 and Ad5-coinfected hamster cells, most of the late structural Ad12 proteins are not made or are made in minimal amounts, and consequently virions are not assembled. It is necessary to investigate whether hamster cells also exhibit a translational block vis à vis the expression of late Ad12-specific mRNAs. The data presented here also demonstrate that Ad12 functions can effectively complement E1A or to a lesser extent E1B deletions in the Ad5 genome in hamster cells. Upon coinfection with Ad12 and deletion mutants of Ad5 in either the E1A or the E1B region, Ad5 DNA and late proteins are synthesized, although Ad5 E1A or E1B functions cannot complement the deficient late Ad12 protein synthesis in hamster cells.