Important note: Information in this article was accurate in 1986. The state of the art may have changed since the publication date.
ROLE OF ONCOGENIC VIRUSES
New Horiz Oncol; 3:33-44 1984. Unique Identifier : AIDSLINE ICDB/86621773 Weiss RA; Inst. of Cancer Res., Royal Cancer Hosp., Chester Beatty Lab.,; London, England
Abstract:
Several viruses can cause cancer in man and animals. These viruses probably induce malignancy by different mechanisms, and interact with different environmental and host cofactors. Malignant disease is a rare result of infection and may occur many years after initial infection. In many cases the viral genome, or a part of it, persists in the tumor cell and may, therefore, contribute directly to its malignant properties; in other malignancies the virus may no longer be present when the tumor appears. There are seven human malignancies in which viruses appear to play an etiological role: Burkitt's lymphoma, immunoblastic lymphoma in renal transplant patients, nasopharyngeal carcinoma, hepatocellular carcinoma, squamous carcinoma (especially uterine cervix), Kaposi's sarcoma, and adult T-cell lymphoma-leukemia. Epstein-Barr virus (EBV) causes infectious mononucleosis, as well as being associated with three kinds of malignancy. Because infection with some of the viruses, eg, EBV, herpes simplex virus, and cytomegalovirus, affects a substantial proportion of the human population whereas the associated cancers are relatively rare, secondary risk factors may play a determining role in the incidence of the disease. A major risk factor in viral carcinogenesis is impairment of the immune system. Wherever viruses prove to the primary cause of cancer, immunization against viral infection must be seriously entertained as a prospect for preventing viral malignancy. Where primary immunization is not practical, intervention at the level of a rate-limiting cofactor could effectively prevent the great majority of viral cancers developing to a clinical presentation. How viruses transform cells into a neoplastic state is not yet understood clearly, although remarkable advances have recently been made in probing the molecular genetics of animal tumor viruses. Tumor viruses could induce neoplasia by a variety of mechanisms, including non-specific tissue damage-inducing proliferation, 'hit-and-run' mutagens, tumor viruses as insertional mutagens, and viral oncogenes. It may be feasible in the not too distant future to exploit our knowledge of oncogenes and their products for the diagnosis and treatment of human cancer. (53 Refs)
Keywords: Burkitt's Lymphoma/MICROBIOLOGY Carcinoma, Hepatocellular/MICROBIOLOGY Carcinoma, Squamous Cell/MICROBIOLOGY Cervix Neoplasms/MICROBIOLOGY Cytomegalovirus/PATHOGENICITY Hepatitis B Virus/PATHOGENICITY Herpesvirus 4, Human Human HTLV-BLV Viruses/PATHOGENICITY Immunologic Deficiency Syndromes Liver Neoplasms/MICROBIOLOGY Lymphoma, Diffuse/MICROBIOLOGY Nasopharyngeal Neoplasms/MICROBIOLOGY Neoplasms/*MICROBIOLOGY Oncogenes Papillomavirus/PATHOGENICITY Retroviridae Infections/MICROBIOLOGY Risk Sarcoma, Kaposi's Tumor Virus Infections/*MICROBIOLOGY JOURNAL ARTICLE REVIEW
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Important note: Information in this article was accurate in 1986. The state of the art may have changed since the publication date.
