RNA tumor viruses, DNA tumor viruses and developmental switches: a unifying hypothesis.
It is hypothesized that oncogenic viruses (both RNA and DNA tumor viruses) use cellular differentiation switches as part of their mechanism for viral replication. Chemical or radiation-induced carcinogenesis is the result of mutations which also affect these differentiation switches and their cellular controls. A transformed cell is characterized by the uncontrolled and inappropriate expression of embryonic (developmental) sequences. Many of the oncogenic viruses, both RNA and DNA, are lineage- and stage-specific in the cells they can productively infect, in keeping with their means of replication. The interaction between virus and host cellular controls determines whether recognizable neoplasia will result from viral infection.
D000818:Animals; D002454:Cell Differentiation; D002472:Cell Transformation, Viral; D004261:DNA Replication; D004263:DNA Tumor Viruses / Q000502:physiology*; D003673:Defective Viruses / Q000502:physiology; D005786:Gene Expression Regulation; D005809:Genes, Regulator; D006378:Helper Viruses / Q000502:physiology; D006801:Humans; D008957:Models, Genetic; D009024:Morphogenesis; D009857:Oncogenes; D012190:Retroviridae / Q000502:physiology*; D014779:Virus Replication