A DNA virus is a virus with genetic materials. They replicate through DNA polymerase. Changes in genes and DNA can course cancer. Genes may cause some faults during different functions that lead t the disease. Some of the genes that may get into an error are the DNA repair genes, ontogenesis, tumor suppressor genes, and self-destruction genes. DNA viruses may cause cancer in the human. The DNA viruses include Epstein - Barr virus, human papillomavirus, hepatitis b virus, and herpesvirus-8. This essay will discuss the DNA virus in cancer and describe the involvement of hepatitis B in cancer formation and development.
DNA virus causes cancer through inactivation of tumor proteins (p53) and retinoblastoma proteins (Rb) (Levine pp. 285-293).When the p53 and Rb inactivate, they allow irregular cell division that ends up causing a tumor. The DNA viruses invade a host cell and integrate their DNA into the cell. The cell dysfunctions when integration takes place. The process is made possible by the bypassing of the GA/s checkpoint and inactivation of the p53 and Rb.
The S phase is tightly regulated as it is the phase where cell replication takes place. The G1 phase prepares the cell before going through mitosis. The p53 an Rb protein controls these two phases. The p53 and Rb make sure that the cell cycle halts until necessary conditions are available and the cell is ready to proceed to the S phase. In this case, the DNA virus prematurely drives the cell into the s phase by inactivating p53 and the Rb.
Different viruses have different ways of inactivating p53. The adenoviruses inactivate p53 by preventing it from binding to the genome. The virus attaches itself on the sites which connect to the genome hence blocking p53 from performing gene regulation. The HPV virus prevents the p53 from gene regulation by degrading it. Rb, on the other hand, is inactivated by viral oncoproteins (Mantovani, and Lawrence, 7874-7887)..
Hepatitis B is a DNA virus that belongs to the hepadnaviridae family. It is a blood-borne pathogen that causes acute and chronic hepatitis. It is also a liver infection that causes hepatocellular carcinoma. The Hepatitis B virus replicates by first attaching itself on a host cell. The virus then gets its DNA into the nucleus of the host cell and start transcription of the cell. The virus uses the polymerase two to perform the transcription and transformation of the cell. For transcription to take place, the relaxed circular genome converted to the covalently closed circular. The CCC required for all viral transcriptions. The cell then infects more cells, and the process repeats itself multiple times. The virus is linked to cancer as it causes mutation of immature cells that create a tumor.
Liver cancer linked to hepatitis B. A patients with the virus is at a higher risk of contacting the hepatocellular carcinoma (HCC) (Michielsen, and E). Hepatitis B causes a tumor that results in the inflammation of the liver. Chronic hepatitis B develops Cancer in most cases. Research has shown that 60% of liver cancer is due to chronic hepatitis B. The risk factors of liver cancer are viral hepatitis, age, heavy alcohol consumption, exposure to certain industrial chemicals and many more.
Many options do the treatment of liver cancer. Ablation, chemotherapy, embolization, immunotherapy, liver transplant radiation, surgical resection, and targeted therapy are all ways fo treating cancer. Ablation is the destruction of cell or tissues. The cell is destroyed through radiofrequency ablation that heats and kills the cell by radio waves and Percutaneous ethanol injection that requires direct injection of alcohol to the liver cells. The radiofrequency ablation destroys small tumors that do not necessarily need surgery or transplant. Embolization involves the destruction of the cancerous cell by blocking the flow of blood to them. blocking blood flow to the affected cells kills them. Embolization can takes place by direct injection of drugs, i.e. Chemoembolization and using radiations called Radioembolization. Immunotherapy in another method of treating cancer that uses the body's immune system. The liver transplant involves removal of the entire liver while surgical resection requires removal of the tumor. Surgical resection is possible when the cancer is still small.
Liver cancer can be prevented by self-education. If an individual diagnosed with hepatitis B., it is his/Her responsibility to live a cautious life. The patient should avoid any behaviors that may increase liver damage. Therefore a patient should know a medical practitioner on how to live a healthy life and prevent the tumor. The hepatitis B vaccine is also a way to prevent one from contracting the virus and cancer. The dose can be given in two or three treatments for 100% protection from the infection. As a risk factor to liver cancer, prevention from the virus will automatically keep one safe from the disease.
Taking frequent screenings for hepatitis B can help keep an individual from cancer. Tumors develop mostly after formation of the chronic hepatitis B., therefore, knowing you Hepatitis status at an early stage and addressing it will help to protect a person from developing liver cancer.
In conclusion, DNA viruses play a significant role in cancer formation. DNA viruses are Epstein - Barr virus, human papillomavirus, hepatitis b virus, and herpesvirus-8. The hepatitis virus is the main risk factor for the development of cancer. It replicates the same way as other DNA viruses. At its acute stage, hepatitis B may not cause cancer. It is effectively treated at the critical stage. When it grows to a chronic phase, the virus can cause tumors that may end up causing cancer. Preventive measures for hepatitis B include taking the vaccine and avoiding all the possible risk factor. When the virus causes disease in the body, cancer can be treated by chemotherapy and radiofrequency waves.
Hepbtalk. "The Link Between Hepatitis B and Liver Cancer." Hepatitis B Foundation, 22 Oct. 2018, www.hepb.org/blog/link-hepatitis-b-liver-cancer/.
Leung, Nancy. "HBV and Liver Cancer." The Medical Journal of Malaysia, U.S. National Library of Medicine, July 2005, www.ncbi.nlm.nih.gov/pubmed/16108176.
Levine, Arnold J. "The Common Mechanisms of Transformation by the Small DNA Tumor Viruses: The Inactivation of Tumor Suppressor Gene Products: p53." Virology, vol. 384, no. 2, 2009, pp. 285-293., doi:10.1016/j.virol.2008.09.034.
Mantovani, Fiamma, and Lawrence Banks. "The Human Papillomavirus E6 Protein and Its Contribution to Malignant Progression." Oncogene, vol. 20, no. 54, 2001, pp. 7874-7887., doi:10.1038/sj.onc.1204869.
Michielsen, P, and E Ho. "Viral Hepatitis B and Hepatocellular Carcinoma." Acta Gastro-Enterologica Belgica, U.S. National Library of Medicine, Mar. 2011, www.ncbi.nlm.nih.gov/pubmed/21563647/.
What Is HBV? biology.kenyon.edu/slonc/bio38/scuderi/parti.html.
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