Oncovirus 1460525 223599769 2008-07-04T20:38:13Z DOI bot 6652755 Citation maintenance. Formatted: title. You can [[WP:DOI|use this bot]] yourself! Please [[User:DOI_bot/bugs|report any bugs]]. 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. ==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 ([[Long terminal repeat|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. ==DNA viruses== *[[JC virus]] has been found in malignant [[colon cancer|colon tumor]]s and may be linked to colon cancer.{{Fact|date=July 2007}} *[[HPV|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]]. *[[Kaposi's sarcoma-associated herpesvirus|Human herpes virus 8]] is associated with [[Kaposi’s sarcoma]], a type of skin cancer (Chang et al., 1994). *[[Epstein-Barr virus|Epstein Barr Virus (EBV)]] is associated with four types of cancers ==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) ==Overview table== {|class=wikitable |- ! Virus ! Associated cancer types |- | Hepatitis viruses, including [[hepatitis B]] and [[hepatitis C]] || [[Hepatocellular carcinoma (liver cancer)]].<ref> {{cite journal |author=Koike K |title=Hepatitis C virus contributes to hepatocarcinogenesis by modulating metabolic and intracellular signalling pathways |journal=J. Gastroenterol. Hepatol. |volume=22 Suppl 1 |issue= |pages=S108–11 |year=2007 |pmid=17567457 |doi=10.1111/j.1440-1746.2006.04669.x}}</ref><ref> {{cite journal |author=Hu J, Ludgate L |title=HIV-HBV and HIV-HCV coinfection and liver cancer development |journal=Cancer Treat. Res. |volume=133 |issue= |pages=241–52 |year=2007 |pmid=17672044 |doi=}} </ref> |- | [[Human T-lymphotropic virus]] || [[Tropical spastic paraparesis]] and [[adult T-cell leukemia]]<ref> {{cite journal |author=Bellon M, Nicot C |title=Telomerase: a crucial player in HTLV-I-induced human T-cell leukemia |journal=Cancer genomics & proteomics |volume=4 |issue=1 |pages=21–5 |year=2007 |pmid=17726237 |doi=}}</ref> |- | [[Human papillomaviruses]] || Cancers of [[cervix]], skin, [[anus]], and [[penis]].<ref> {{cite journal |author=Schiffman M, Castle PE, Jeronimo J, Rodriguez AC, Wacholder S |title=Human papillomavirus and cervical cancer |journal=Lancet |volume=370 |issue=9590 |pages=890–907 |year=2007 |pmid=17826171 |doi=10.1016/S0140-6736(07)61416-0}}</ref> |- | [[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]].<ref> {{cite journal |author=Klein E, Kis LL, Klein G |title=Epstein-Barr virus infection in humans: from harmless to life endangering virus-lymphocyte interactions |journal=Oncogene |volume=26 |issue=9 |pages=1297–305 |year=2007 |pmid=17322915 |doi=10.1038/sj.onc.1210240}}</ref> |} == 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 [[1950]]s 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.<ref name="zur Hausen-viruses">{{cite journal | author = zur Hausen H | title = Viruses in human cancers | journal = Science | volume = 254 | issue = 5035 | pages = | year = 1991 | pmid = }}</ref> 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 [[retrovirus]]es, 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 [[Hepatocellular carcinoma|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 [[Centers for Disease Control and Prevention|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. ==See also== * [[carcinogen]] * [[oncogenic]] * [[oncogene]] * [[Adult T-cell leukemia/lymphoma]] * [[Cancer bacteria]] {{Viruses}} ==References== {{Reflist}} ==Further reading== Chang et al. (1994). Identification of herpesvirus-like DNA sequences in AIDS-associated Kaposi's sarcoma. Science 266:1865-1869. <br />Scheffner et al. (1990). The E6 oncoprotein encoded by human papillomavirus types 16 and 18 promotes the degradation of p53. Cell 63:1129-1136. ==External links== * {{MeshName|Oncoviruses}} [[Category:Viruses]] [[Category:Oncology]] [[Category:Virology]] [[Category:Microbiology]] [[ca:Oncovirus]] [[de:Onkovirus]] [[es:Oncovirus]] [[fr:Oncovirus]] [[it:Oncovirus]] [[pl:Wirusy onkogenne]]