Important note: Information in this article was accurate in 1985. The state of the art may have changed since the publication date.
CONSIDERATIONS OF VIRAL ETIOLOGY: CAUSES AND EFFECTS
AIDS. The Epidemic of Kaposi's Sarcoma and Opportunistic Infections. Friedman-Kien AE, Laubenstein LJ, eds. New York, Masson, p. 101-10, 1984.. Unique Identifier : AIDSLINE ICDB/85610695 Pagano JS; Cancer Res. Center, Univ. of North Carolina, Chapel Hill, NC; 27514
Abstract:
Evidence and hypotheses regarding viral etiologies of Kaposi's sarcoma (KS) and the Acquired Immune Deficiency Syndrome (AIDS) are discussed. Viruses implicated (with varying degrees of certainty) in human tumors include human T-cell leukemia viruses, papillomavirus, papova viruses, adenovirus, herpes simplex II, cytomegalovirus (CMV), Epstein-Barr virus (EBV), and hepatitis B virus. Virus-induced cancers are generally uncommon and sporadic, and cofactors are suspected in endemic areas. The oncogenic viruses are characterized by RNA or DNA genomes, circular or pro-viral genomes, retention of viral genes in the host cell, viral stimulation of host macromolecule synthesis, nonlytic infection, and tissue-proliferative effects. EBV infection has been hypothesized to cause AIDS but is more likely a consequence of immune dysfunction. Lymphoproliferation is frequent in EBV infection, probably as a result of secondary infection of B lymphocytes with the virus, and may be enhanced by impaired cellular immunity. Potential therapies for EBV-associated lymphoproliferative disease include antiviral agents, radiotherapy, or monoclonal antibodies. AIDS may be the result of primary infection with an AIDS virus (which impairs cellular immunity and permits secondary infection), EBV-triggered lymphoproliferation, KS, and, perhaps, other malignancies. The KS may result from reactivation of a prior virus infection, perhaps CMV. The AIDS virus is hypothesized to be a new virus with multimodal transmission, which may commonly cause silent infection in the general population and may infect the T-cell secondarily. Given the identification of epidemic acquired immune deficiency in monkeys, a crossover infection from simian infections is also possible. (27 Refs)
Keywords: Acquired Immunodeficiency Syndrome/COMPLICATIONS/*ETIOLOGY/ TRANSMISSION Animal Cytomegalovirus Herpesvirus 4, Human Human Lymphoma/*ETIOLOGY Receptors, Virus Sarcoma, Kaposi's/*ETIOLOGY T-Lymphocytes/MICROBIOLOGY *Tumor Virus Infections MEETING PAPER REVIEW
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Important note: Information in this article was accurate in 1985. The state of the art may have changed since the publication date.
