Interactions between tumour-viruses and genetic components of the cell
In the 1960s Dulbecco studied the effect of a simple DNA virus on cultured animal cells. He found that when the virus inserted its own genetic code into that of the cell during replication, it either destroyed the cell, releasing viral particles, or transformed it to a cancer cell. Further experiments showed that the viral DNA remained within the transformed cells, giving the tumours virus-like properties, such as unlimited growth.
Howard Temin investigated the role of RNA viruses in tumour development. He proposed that RNA tumour viruses could generate DNA, which could then be incorporated into the cell. The idea that a DNA copy could be made from RNA reversed the usual principle that DNA is copied into RNA.
At MIT, Baltimore had studied the polio virus for many years, but in 1969 he began to investigate other RNA viruses, including Rous sarcoma virus. In 1970 Baltimore and Temin independently discovered reverse transcriptase, which is a viral enzyme that produces DNA from an RNA template. Dulbecco’s mechanism of transformation applied to both DNA and RNA tumour viruses, and we now know that many animal and human cancers can be caused by viruses.
These discoveries came from work in animal cell lines and cell cultures, and the production of normal and cancerous tissue in animals including monkey, horse, chicken and mouse. This research led directly to the development of vaccines for animal cancers such as feline leukaemia, and, more recently human cervical cancer. It has helped us understand retroviruses such as HIV.