Adenoviruses and human tumors: regulation of eukaryotic chromatin structure?

Adenoviruses possess four early gene clusters. E1A, and E1B sequences are directly involved in the initiation of transformation of both rodent, and human cells. Oncogenic potential of the in vitro immortalized rodent cells is also dependent on the expression of E1A, and E1B. Genes E2A, and E2B are coding for DNA-binding proteins. These regions may influence the frequency of in vitro transformation if complete virions were used for the immortalization of rodent cells. The existence of the E3 gene cluster, which has been shown to be non-essential to the productive replication in certain host cells, is unique for the adenovirus family. Foreign DNA fragments inserted into E3 or replacing it may modify the host range of adenovirus, and may initiate oncogenic transformation of rodent cells. May cellular oncogenes replace the non-essential region of the adenoviral genome? Are host-range modifications, the formation of defective genomes, and interactions of viral, and cellular DNA in vivo biological properties of adenoviruses? These questions are discussed in the light of recent findings concerning virus-coded functions which may modify chromatin structure, and may be associated with oncogenic potential of adenoviruses in the natural hosts.