Studies of Small DNA Virus Encoded Oncogenes in Viral Carcinogenesis Using Laboratory Model Systems

Cancer is a devastating disease, presenting an immense disease burden to affected individuals and their families as well as health care systems with 10.9 million new cases and 6.7 million deaths per year. Approximately 12% of human cancers worldwide are caused by oncoviruses infection with more than 80% of cases occurring in the developing world.

Tumor viruses can be classified into two groups based on their genetic material;

1. DNA tumor viruses:

2. Small DNA tumor viruses (Papilloma viruses, Polyoma viruses and adenoviruses).

3. Complex DNA tumor viruses (Herpes viruses and Hepatitis B viruses).

4. RNA tumor viruses ( Hepatitis C viruses and human T-cell leukemia virus "HTLV").

There are around 100 types of HPV, with different variations in their genetic and oncogenic potential [5]. Thus, HPV genotypes are divided into 2 groups based on their vulnerability; High risk HPV (HR-HPV) and low risk HPV (LR-HPV).

The HPV genome encodes several oncoproteins [5]. E6 and E7 are the main genes responsible for cell transformation mediated by HR-HPV, and they modulate the activities of cellular proteins that regulate the cell cycle. Thus, the presence of E6/E7 can be a specific marker for diagnosing precancerous lesions by HPV.

Knowledge of the etiology of virus-mediated carcinogenesis, the networking of pathways involved in the transition from infection to cancer and the risk factors associated with each type of cancer, all suggest prophylactic and therapeutic strategies that may reduce the risk of virus-mediated cancer.