Important note: Information in this article was accurate in 1991. The state of the art may have changed since the publication date.
HUMAN T-CELL LEUKEMIA VIRUS, TYPE 1, AND HUMAN LEUKEMIA AND LYMPHOMA
Molecular Genetics in Cancer Diagnosis. Cossman J, ed. New York, Elsevier, p. 163-78, 1990.. Unique Identifier : AIDSLINE ICDB/91676250 Reitz MS; Lab. of Tumor Cell Biology, NCI, Bethesda, MD
Abstract:
Human T-cell leukemia virus, type 1 (HTLV-1), was the first human retrovirus discovered. It is the etiologic agent of adult T-cell leukemia/lymphoma (ATL), a distinct form of leukemia/lymphoma recognized first in Japan. Reagents from HTLV-1 have aided in the diagnosis of this disease and been instrumental in its definition as a worldwide clinical entity. HTLV-1 and human leukemia and lymphoma are reviewed under the following headings: isolation of HTLV-1, HTLV-1 and ATL, possible mechanisms of leukemogenesis, infection of cells in vitro, viral regulatory genes, other disease associations, other human retroviruses, and prospects for control of HTLV-1. After the link between ATL and HTLV-1 was first established in Japan, where more than 90% of ATL samples were positive for serum antibodies to HTLV-1, a similar clinical entity in the Caribbean and England was shown to be strongly associated with HTLV-1 seropositivity. Routes of transmission are sexual (predominantly male to female), from mother to infant via breast feeding, and through blood products. The seroepidemiological evidence overwhelmingly shows that HTLV-1 is the causative agent of ATL, but the precise way in which the virus induces the disease is far from clear. HTLV-1 is a more complex retrovirus than many of the animal retroviruses in its genomic structure and possibly in its mechanism of leukemogenesis. The presence of genetic information in addition to gag, pol, and env genes and the long terminal repeat in HTLV-1 is analogous to the acutely transforming retroviruses, but unlike these viruses, the extra genetic material is not derived from the host cell. At least two possible viral regulatory proteins have been identified that control virus behavior in cells. In the presence of the protein coded by the rex gene, the expression of viral structural proteins increases, but because rex also decreases the levels of spliced mRNA, its expression would decrease synthesis of both tax (the gene associated with transformation) and rex. This in turn would lead to a decrease in total viral RNA and consequently to a decrease in viral structural proteins. Other human retroviruses are now known, including HTLV-2 (T-cell variant of hairy cell leukemia), HIV-1 (AIDS), and HTLV-5 (some non-ATL cases of cutaneous T-cell lymphoma). Knowledge of the HTLV-1 routes of transmission suggests methods of prevention; a vaccine based on HTLV-1 proteins has been tested successfully in cynomolgus monkeys. (59 Refs)
Keywords: Cell Transformation, Viral/GENETICS Gene Expression Regulation, Leukemic/*PHYSIOLOGY Gene Expression Regulation, Viral/*PHYSIOLOGY Genes, Viral/GENETICS Human HTLV-I/*GENETICS Leukemia-Lymphoma, T-Cell, Acute, HTLV-I-Associated/*GENETICS T-Lymphocytes/MICROBIOLOGY Transcription, Genetic/GENETICS MONOGRAPH REVIEW 912130
M91C4102
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Important note: Information in this article was accurate in 1991. The state of the art may have changed since the publication date.
