Tumor viruses

Tumor viruses

Viruses associated with tumors can be classified in two broad categories depending on the nucleic acid in the viral genome and the type of strategy to induce malignant transformation.

RNA viruses

The ribonucleic acid (RNA) tumor viruses are retroviruses. When they infect cells, the viral RNA is copied into deoxyribonucleic acid (DNA) by reverse transcription and the DNA is inserted into the host genome, where it persists and can be inherited by subsequent generation of cells. Transformation of the infected cells can be traced to oncogenes that are carried by the viruses but are not necessary for viral replication. The viral oncogenes are closely similar to cellular genes, the proto-oncogenes, which code for components of the cellular machinery that regulates cell proliferation, differentiation, and death. Incorporation into a retrovirus may convert proto-oncogenes into oncogenes in two ways: the gene sequence may be altered or truncated so that it codes for proteins with abnormal activity; or the gene may be brought under the control of powerful viral regulators that cause its product to be made in excess or in inappropriate circumstances. Retroviruses may also exert similar oncogenic effects by insertional mutation when DNA copies of the viral RNA are integrated into the host-cell genome at a site close to or even within proto-oncogenes. See Retrovirus

RNA tumor viruses cause leukemias, lymphomas, sarcomas, and carcinomas in fowl, rodents, primates, and other species. The human T-cell leukemia virus (HTLV) types I and II are endemic in Southeast Asian populations and cause adult T-cell leukemia and hairy-cell leukemia.

DNA viruses

DNA viruses replicate lytically and kill the infected cells. Transformation occurs in nonpermissive cells where the infection cannot proceed to viral replication. The transforming ability of DNA tumor viruses has been traced to several viral proteins that cooperate to stimulate cell proliferation, overriding some of the normal growth control mechanisms in the infected cell and its progeny. Unlike retroviral oncogenes, DNA virus oncogenes are essential components of the viral genome and have no counterpart in the normal host cells. Some of these viral proteins bind to the protein products of two key tumor suppressor genes of the host cells, the retinoblastoma gene and the p53 gene, deactivating them and thereby permitting the cell to replicate its DNA and divide. Other DNA virus oncogenes interfere with the expression of cellular genes either directly or via interaction with regulatory factors. There is often a delay of several years between initial viral infection in the natural host species and the development of cancer, indicating that, in addition to virus-induced transformation, other environmental factors and genetic accidents are involved. A specific or general impairment of the host immune responses often plays an important role.

DNA tumor viruses belong to the families of papilloma, polyoma, adeno, hepadna, and herpes viruses and produce tumors of different types in various species. DNA tumor viruses are thought to play a role in the pathogenesis of about 15–20% of human cancers. These include Burkitt's lymphoma, nasopharyngeal carcinoma, immunoblastic lymphomas in immunosuppressed individuals and a proportion of Hodgkin's lymphomas that are all associated with the Epstein-Barr virus of the herpes family; and liver carcinoma associated with chronic hepatitis B virus infection. See Animal virus, Epstein-Barr virus, Mutation

McGraw-Hill Concise Encyclopedia of Bioscience. © 2002 by The McGraw-Hill Companies, Inc.
References in periodicals archive ?
Avian tumor viruses: persistent and evolving pathogens.
Human tumor viruses carry oncogenes which when incorporated into host cell are usually responsible for transformation of target cells by expression of oncoproteins and alteration in cellular machinery3.
For now, many DNA tumor viruses are known; they are grouped in four families, namely, SV40 and polyomavirus, papilloma viruses (HPV), adenoviruses, and herpesviruses.
They discuss biogenesis and applications of microRNA; non-canonical microRNA biogenesis and function; non-coding RNAs and the epigenetic control of gene expression; the clinical translation of microRNA technologies for somatic cell reprogramming; systems biology tools for understanding the role of host microRNAs in infection, particularly in HIV; synthetic microRNA blocking agents; using microRNAs to regulate transgene expression, for gene silencing, and using RNAi for the treatment of viral infections; the role of microRNAs in cancers associated with human tumor viruses; microRNAs as cancer biomarkers; and microRNA deregulation in trinucleotide repeat expansion disorders.
Small DNA tumor viruses: large contributors to biomedical sciences.
Cancer transcriptomes often have rearranged genomes and harbor transcripts that are not encoded in a reference genome, like those derived from tumor viruses or microbes.
Beginning at the "dawn of molecular biology" in the 1930s-40s, selected vignettes give the background behind the discovery of DNA tumor viruses, advances in understanding cell cycle regulation, repair and replication mechanisms, and apoptosis, and unexpected insights from such places as Klinefelter's syndrome and Drosophila mutations.
Steinberg did a fellowship studying mammalian tumor viruses at the State University of New York, Stony Brook.
Immunodeficiency (whether congenital, iatrogenic, or caused by infection) increases the risk of some types of cancer, especially malignancies etiologically linked to DNA tumor viruses, such as herpesviruses and polyomavirus.
A sense of personal responsibility motivated him to raise the safety issue, he says, explaining that even if he could accept a small chance of danger, he realized that the people working around him might not be so "gung ho." Recalling a meeting in 1973 where scientists considered the potential risks in working with tumor viruses, he says there was already a feeling that "some things might be dangerous.
Finally, we discuss the biological evidence or lack thereof that avian tumor viruses are involved in the etiology of human cancer and multiple sclerosis (MS).

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