A number of viruses are suspected of causing cancer in animals, including humans, and are frequently referred to as oncogenic viruses. Examples include human papillomaviruses, the Epstein-Barr virus, and the hepatitis B virus, all of which have genomes made up of DNA. Human T-cell leukemia virus type I (HTLV-I), which is a retrovirus (a type of RNA virus), is linked to tumour formation in humans.

The molecular mechanisms of viral oncogenesis are complex and may involve the induction of chronic inflammation, disruption of host genetic and epigenetic integrity and homeostasis, interference with cellular DNA repair mechanisms resulting in genome instability and cell cycle dysregulation. Oncogenic DNA viruses can also insert their genomic DNA into cellular chromosomes, resulting in genetic abnormity.

Viral ‘oncoproteins’ can activate cellular signaling pathways, alter the expression of cellular genes and microRNAs either transcriptionally or post-transcriptionally, and destabilize or inactivate tumor suppressor proteins and proteins that regulate cell polarity, signal transduction, immune response, and apoptosis. Genetic and epigenetic alterations induced by infection and replication of oncogenic viruses may lead to the appearance and proliferation of cancer stem cells, which are important for the initiation, progression, metastasis, relapse, and chemotherapy resistance of cancers.

The importance and underlying molecular mechanisms of specific cellular genes and signaling pathways in viral oncogenesis are subjects of intense research efforts. A great deal of new knowledge on viral oncogenesis has been obtained through the studies of virus-induced tumorigenicity in xenograft animal models. More significantly, a number of new drugs and vaccines have been developed for treatment and prevention of virus-induced cancers.

Media Contact:

Sophie Kate
Managing Editor
Microbiology: Current Research
Email: aamcr@alliedacademies.org