Oncovirus
From Wikipedia, the free encyclopedia
An oncovirus is a virus associated with cancer.
Oncoviruses come in two different forms: viruses with a DNA genome, such as adenovirus, and viruses with an RNA genome, like the Human T-cell Leukemia viruses and several viruses known to be common in cats, mice and chickens.
The oncogenic mechanism is either to insert additional oncogenic genes in the host DNA, or to enhance already existing oncogenic genes in the genome.
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[edit] Mechanism
Some oncogenic retroviruses i.e. cancer-causing viruses with RNA genomes, insert their genome into the host cell and use reverse transcriptase to make DNA. This DNA is then incorporated into the cell DNA along with powerful promoter sequences (LTRs) that promote transcription of the viral DNA to reproduce more virus. However, sometimes the viral DNA incorporates a section of the host DNA which contains genes for growth promotion. These growth genes, sometimes called proto-oncogenes in their normal state, become oncogenic once incorporated into the viral DNA because of the increased transcription caused by the viral LTRs. This causes increased growth of the infected cell, leading to cellular proliferation and the formation of tumors. Numerous oncogenes have been discovered in the genomes of transforming retroviruses.
Other oncogenic retroviruses transform cells by integrating into the host gene near a proto-oncogene. If the viral LTRs are close enough to that oncogene, they will upregulate transcription not only of the viral DNA but of the proto-oncogene nearby, causing growth, cell proliferation and by consequence tumour formation.
[edit] DNA viruses
- JC virus has been found in malignant colon tumors and may be linked to colon cancer.[citation needed]
- Human Papilloma Virus (HPV), a DNA virus, causes transformation in cells through interfering with tumor suppressor proteins such as p53. Interfering with the action of p53 allows a cell infected with the virus to move into a different stage of the cell cycle allowing the virus genome to be replicated forcing the cell into the S phase of the cell cycle could cause the cell to become transformed (Scheffner et al., 1990). It increases risk of e.g. cervical cancer.
- Human herpes virus 8 is associated with Kaposi’s sarcoma, a type of skin cancer (Chang et al., 1994).
- Epstein Barr Virus (EBV) is associated with four types of cancers
[edit] RNA viruses
It is not only DNA viruses that are associated with cancers some RNA viruses have also been associated such as the Hepatitis C Virus as well as Human T cell leukaemia virus-1 (HTLV-1)
[edit] Overview table
| Virus | Associated cancer types |
|---|---|
| Hepatitis viruses, including hepatitis B and hepatitis C | Hepatocellular carcinoma (liver cancer).[1][2] |
| Human T-lymphotropic virus | Tropical spastic paraparesis and adult T-cell leukemia[3] |
| Human papillomaviruses | Cancers of cervix, skin, anus, and penis.[4] |
| Kaposi’s sarcoma-associated herpesvirus | Kaposi’s sarcoma and Body cavity lymphoma |
| Epstein–Barr virus | Burkitt’s lymphoma, Hodgkin’s lymphoma, B lymphoproliferative disease and Nasopharyngeal carcinoma.[5] |
[edit] History
The theory that cancer could be caused by a virus began to be developed in 1911 by Peyton Rous. Rous transmitted solid tumors of chickens by transplanting tissue between them.
By the early 1950s it was known that viruses could remove and incorporate genes and genetic material in cells. It was suggested that these new genes inserted into cells could make the cell cancerous. Many of these viral oncogenes have been discovered and identified to cause cancer.
The main viruses associated with human cancers are human papillomavirus, hepatitis B and hepatitis C virus, Epstein-Barr virus, and human T-lymphotropic virus. Experimental and epidemiological data imply a causative role for viruses and they appear to be the second most important risk factor for cancer development in humans, exceeded only by tobacco usage.[6] The mode of virally-induced tumors can be divided into two, acutely-transforming or slowly-transforming. In acutely transforming viruses, the viral particles carry a gene that encodes for an overactive oncogene called viral-oncogene (v-onc), and the infected cell is transformed as soon as v-onc is expressed. In contrast, in slowly-transforming viruses, the virus genome is inserted, especially as viral genome insertion is an obligatory part of retroviruses, near a proto-oncogene in the host genome. The viral promoter or other transcription regulation elements in turn cause overexpression of that proto-oncogene, which in turn induces uncontrolled cellular proliferation. Because viral genome insertion is not specific to proto-oncogenes and the chance of insertion near that proto-oncogene is low, slowly-transforming viruses have very long tumor latency compared to acutely-transforming viruses, which already carry the viral oncogene.
Hepatitis viruses, including hepatitis B and hepatitis C, can induce a chronic viral infection that leads to liver cancer in 0.47% of hepatitis B patients per year (especially in Asia, less so in North America), and in 1.4% of hepatitis C carriers per year. Liver cirrhosis, whether from chronic viral hepatitis infection or alcoholism, is associated with the development of liver cancer, and the combination of cirrhosis and viral hepatitis presents the highest risk of liver cancer development. Worldwide, liver cancer is one of the most common, and most deadly, cancers due to a huge burden of viral hepatitis transmission and disease.
Advances in cancer research have made a vaccine designed to prevent cancer available. In 2006, the US FDA approved a human papilloma virus vaccine, called Gardasil. The vaccine protects against four HPV types, which together cause 70% of cervical cancers and 90% of genital warts. In March 2007, the US CDC Advisory Committee on Immunization Practices (ACIP) officially recommended that females aged 11-12 receive the vaccine, and indicated that females as young as age 9 and as old as age 26 are also candidates for immunization.
[edit] See also
[edit] Viruses templates
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[edit] References
- ^ Koike K (2007). "Hepatitis C virus contributes to hepatocarcinogenesis by modulating metabolic and intracellular signalling pathways". J. Gastroenterol. Hepatol. 22 Suppl 1: S108–11. doi:. PMID 17567457.
- ^ Hu J, Ludgate L (2007). "HIV-HBV and HIV-HCV coinfection and liver cancer development". Cancer Treat. Res. 133: 241–52. PMID 17672044.
- ^ Bellon M, Nicot C (2007). "Telomerase: a crucial player in HTLV-I-induced human T-cell leukemia". Cancer genomics & proteomics 4 (1): 21–5. PMID 17726237.
- ^ Schiffman M, Castle PE, Jeronimo J, Rodriguez AC, Wacholder S (2007). "Human papillomavirus and cervical cancer". Lancet 370 (9590): 890–907. doi:. PMID 17826171.
- ^ Klein E, Kis LL, Klein G (2007). "Epstein-Barr virus infection in humans: from harmless to life endangering virus-lymphocyte interactions". Oncogene 26 (9): 1297–305. doi:. PMID 17322915.
- ^ zur Hausen H (1991). "Viruses in human cancers.". Science 254 (5035).
[edit] Further reading
Chang et al. (1994). Identification of herpesvirus-like DNA sequences in AIDS-associated Kaposi's sarcoma. Science 266:1865-1869.
Scheffner et al. (1990). The E6 oncoprotein encoded by human papillomavirus types 16 and 18 promotes the degradation of p53. Cell 63:1129-1136.
