Important note: Information in this article was accurate in 1992. The state of the art may have changed since the publication date.
BIOLOGY OF HUMAN T-CELL LEUKEMIA VIRUS (HTLV) INFECTION
The Human Retroviruses. Gallo RC and Jay G, eds. San Diego, Academic Press, p. 109-25, 1991.. Unique Identifier : AIDSLINE ICDB/92678723 Miyoshi I; Dept. of Medicine, Kochi Medical Sch., Kochi 783, Japan
Abstract:
Since the first discovery of murine leukemia virus, RNA tumor viruses (retroviruses) have been implicated in the etiology of many naturally-occurring leukemias and lymphomas in various animal species. Extensive studies have confirmed the etiological role of HTLV-I in adult T-cell leukemia (ATL); HTLV-I also has been linked to tropical spastic paraparesis (TSP) or HTLV-I-associated myelopathy (HAM). HTLV-II has been isolated from patients with a T-cell variant of hairy-cell leukemia. The biology of HTLV infection is reviewed including biological activity of HTLV-I in vitro; transmission of HTLV-I to monkeys; transmission of HTLV-I to rabbits (inoculation of HTLV-I-producing cells and cell-free virus, transmission by blood transfusion, oral transmission, and mother-to-offspring transmission); and active and passive immunization against HTLV-I in rabbits. HTLV-I has a unique property of infecting and immortalizing not only human T cells, but the T cells of various species of animals in vitro. Moreover, the virus infects monkeys and rabbits, rendering them seropositive virus carriers as in humans. The rabbit model has proved particularly useful for demonstrating the transmission routes of HTLV-I, although no virus-induced disease, hematological or neurological has been observed so far. For full control of ATL and TSP/HAM, more progress must be made in understanding virus infection, pathogenesis, and treatment. First, it is important to interrupt the routes of virus transmission from one generation to the next. The author's passive immunization experiment in rabbits suggests that neutralizing antibody is effective in preventing cell-to-cell infection of HTLV-I. If this is the case, it will be necessary to clarify the level and duration of the protection in babies provided by maternally transmitted antibodies. It ultimately may be possible to administer HTLV-I immune globulin or a vaccine capable of inducing neutralizing antibody under certain circumstances. Two other steps necessary for HTLV-I control are obtaining a better understanding of the mechanism of viral leukemogenesis and myelopathy development to enable prediction of disease among asymptomatic virus carriers and development of a new approach to therapy yielding improved patient survival and prognosis. (93 Refs)
Keywords: Animal Cell Transformation, Neoplastic/GENETICS/IMMUNOLOGY Cell Transformation, Viral/*GENETICS/IMMUNOLOGY/PHYSIOLOGY Female Gene Expression Regulation, Viral/*PHYSIOLOGY Haplorhini Human HTLV-I/*GENETICS/IMMUNOLOGY/PATHOGENICITY Immunization, Passive Infant, Newborn Leukemia-Lymphoma, T-Cell, Acute, HTLV-I-Associated/*GENETICS/ IMMUNOLOGY/MICROBIOLOGY/TRANSMISSION Pregnancy Rats T-Lymphocytes/IMMUNOLOGY/MICROBIOLOGY Vaccination Virus Replication/*GENETICS/PHYSIOLOGY MONOGRAPH REVIEW
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Important note: Information in this article was accurate in 1992. The state of the art may have changed since the publication date.
