IV. VIRUSES
F. ANIMAL VIRUS LIFE CYCLES
5. The Role of Viruses in Tumor Production
The overall purpose of this Learning Object is to understand the role a few viruses play in increasing the risk for certain cancers.
Viruses are infectious agents with both living and nonliving characteristics.
1. Living characteristics of viruses
a. They reproduce at a fantastic rate, but only in living host cells.
b. They can mutate.
2. Nonliving characteristics of viruses
a. They are acellular, that is, they contain no cytoplasm or cellular organelles.
b. They carry out no metabolism on their own and must replicate using the host cell's metabolic machinery. In other words, viruses don't grow and divide. Instead, new viral components are synthesized and assembled within the infected host cell.
c. The vast majority of viruses possess either DNA or RNA but not both.
The Role of Viruses in Tumor Production
Some viruses can also play a role in converting normal host cells into tumor cells. These viruses are capable of viral transformation, that is, they transform normal cells into malignant cells. In fact, five viruses, hepatitis B virus (HBV), hepatitis C virus (HCV), human papilloma virus (HPV), Epstein-Barr virus (EBV), and human T-lymphotropic virus type I (HTLV-I) are thought to contribute to over 15% of the world's cancers. Up to 80% of these human viral-associated cancers are cervical cancer (associated with HPV) and liver cancer (associated with HBV and HCV).
The hepatitis B virus (HBV) is a DNA virus that may potentially cause chronic (def) hepatitis in those infected. There is a strong link between chronic infection with HBV and hepatocellular carcinoma (def), which typically appears after 30-50 years of chronic liver damage and liver cell replacement. Approximately 90% of infected infants and 30% of infected children less than 5 years of age become chronically infected. Only 2%–6% of infected adults become chronically infected. The risk of death from cirrhosis or hepatocellular carcinoma in those chronically infected with HIV is 15%–25%. HBV is transmitted by blood and blood products, sexually, and perinatally from an infected mother to her baby. There are about one million chronic carriers of HBV in the US. Worldwide, HBV is responsible for 60% of all liver cancer cases.
The hepatitis C virus (HCV) is a RNA virus that may also cause chronic hepatitis in those infected. As with HBV, there is a strong link between chronic infection with HCV and liver cancer, typically appearing after 30-50 years of chronic liver damage and liver cell replacement. Between 70% and 85% of individuals infected with HCV become chronic carriers and there are approximately 3.2 million chronic carriers of HCV in the US. HCV is transmitted primarily by by blood and blood products and less commonly, sexually. Worldwide, HCV is responsible for 22 % of all liver cancer cases.
The human papilloma viruses (HPV) are responsible for warts. While warts are generally considered as benign tumors, some sexually-transmitted strains of HPV are associated with several cancers. For example, HPV-16 and and HPV-18 are responsible for approximately 70% of cervical cancer in the US. HPV has also been implicated in vulvar cancer, vaginal cancer, anall cancer, and squamous cell carcinoma of the penis. In these tumor cells the viral DNA is usually found integrated in host cell chromosomes. In the US, HPVs are associated with almost all deaths due to cervical cancer each year.
The Epstein-Barr virus (EBV), a herpes virus, normally causes benign proliferations such as infectious mononucleosis and hairy leukoplakia of the tongue. However, it can contribute to nonHodgkin's lymphoma in AIDS patients and post-transplantation lymphoproliferative diseases, appears to be an essential factor for posterior nasopharyngeal cancer in some individuals, can be a co-factor for Burkitt's lymphoma, and contributes to smooth-muscle tumors in immunosuppressed children. EBV is typically spread by saliva and approximately 90% of adults have been exposed.
The retrovirus human T-lymphotropic virus type I (HTLV-I) can induce a rare adult T-lymphocyte leukemia-lymphoma. It is transmitted by blood and blood products, sexually, and perinatally from an infected mother to her baby.
The development of tumors is a multistep process depending on the accumulation of mutations altering a number of genes. The altered genes then function collectively to cause malignant growth.
Proliferation of normal cells is regulated by growth-promoting proto-oncogenes (def) and counterbalanced by growth-restricting tumor suppressor genes (def). Mutations that increase the activities of proto-oncogenes to create oncogenes (def) and/or decrease the activities of tumor suppressor genes can lead to growth of tumors. It is now known that many tumors require both activation of oncogenes from proto-oncogenes and inactivation of tumor suppressor genes for their development.
Viruses are thought to play a role in cancer development both indirectly and directly. Indirectly, the viruses may induce immunosuppression so that cancer cells are not removed by immune responses, as in the case of HIV/AIDS, or they may cause long term damage to tissues resulting in large scale cell regeneration which increases the chances of natural mutation in proto-oncogenes and tumor suppressor genes, as in the case of HBV and HCV. Directly, by integrating into the host cell's chromosomes, some viruses may alter the normal function of the proto-oncogenes and tumor suppressor genes, as is seen with HPV and HBV.
However, most virus-associated cancers have long latency periods of several decades and only a small percentage of the people infected with the virus actually develop the cancer. This indicates other factors promoting changes in cellular genes are also involved. For example, in the case of cervical cancer and HPV, two varients of a tumor suppressor gene known as p53 are known. One form of the p53 gene produces a suppressor protein that is much more susceptible to degradation by an oncoprotein called E6 which is produced by carcinogenic strains of HPV.
E-Medicine article on infections associated with organisms mentioned in this Learning Object. Registration to access this website is free.
Student-Authored Descriptions of Viral Infections
Astroviruses by Michele Stedding
Coxsackievirus by Mandy Hughes
Coxsackievirus by Salyna Riggs
Cytomegalovirus (CMV) by Cindi Chou
Ebola by Christine Sprinkle
Ebola by Dianne Bettick
Ebola by LaTanya Gary
Epstein-Barr Virus (EBV) by Erica Rome
Hantavirus by Jennifer Robinson
Hepatitis A (HAV) by Anastasiya Lyudkevich
Hepatitis B (HBV) by Karen Neff
Hepatitis C (HCV) by Rosemary Bewley
Hepatitis C (HCV) by Corinne Borel
Herpes Simplex types 1 and 2 (HSV1 &HSV2) by Katrina Armstrong
Herpes Simplex types 1 and 2 (HSV1 & HSV2) by Cindy Dubs
Herpes Simplex type 2 ( HSV2) by Lauren Bentley
Human Immunodeficiency Virus (HIV) by Steven Merrill
Human Papilloma Viruses (HPV) by Megan Johnson
Human Papilloma Virus (HPV) by Laura Moy
Influenza by Kenneth Agboifo
Measles (Rubeola) by Peggy Engel
Measles (Rubeola) by Sumara Choudhry
Measles (Rubeola) by Yashu Karki
Mumps by Trudy Ann Hinds
Noroviruses by Kristina Garner
Poliomyelitis by Deborah Malin
Rabies by Pamela Russillo
Rabies by Lauren Mekalian
Rhinoviruses (colds) by Nina Mezu
Rift Valley Fever by LaWanda Morgan
Respiratory Syncytial Virus (RSV) by Ben Kaufman
Respiratory Syncytial Virus (RSV) by Christen Strickler
Rotaviruses by Chrissy Blake
Rotaviruses by Shana Lucas
Varicella (chickenpox) by Rosemary Brunet
Varicella (chickenpox) by Violeta Genova
Viral Meningitis by Denise Grandea
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Updated: March, 2011
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