Important note: Information in this article was accurate in 1991. The state of the art may have changed since the publication date.
MOLECULAR BIOLOGY AND PATHOGENESIS OF HTLV-II
Retrovirus Biology and Human Disease. Gallo RC and Wong-Staal F, eds. Marcel Dekker, New York, p. 187-207, 1990.. Unique Identifier : AIDSLINE ICDB/91676224 Cann AJ; Rosenblatt JD; Wachsman W; Chen IS; Dept. of Medicine, UCLA Sch. of Medicine, Los Angeles, CA
Abstract:
Comparative molecular biology of human T-cell leukemia virus type 1 (HTLV-I) and HTLV-II affords the opportunity to investigate the pathogenesis of these viruses. The authors' molecular studies of HTLV-II are reviewed and related to unanswered questions concerning the mechanism of cell transformation by HTLV and the biology of HTLV infection. Topics include the following: structure of the HTLV-II genome, expression of viral genes, transactivation of transcription, cell transformation in vitro, and biology of HTLV-II infection. Both viruses have a similar genetic organization and share approx 60% overall nucleotide sequence homology. However, despite their evident relatedness, the pathology of the diseases with which they are associated is distinct. The tax gene was thought to be involved in leukemogenesis when it was first identified, and the discovery that the tax protein is a transcriptional activator led to the hypothesis that it was involved in cell transformation by causing aberrant transcriptional regulation in infected cells. The authors' studies have revealed that the HTLV-II tax protein can activate transcription from heterologous promoters and that the capabilities of tax protein in control of viral gene expression are complex. These results suggest mechanisms of cellular transformation other than aberrant transcriptional activation. For HTLV-II replication, p37(taxI) is required and is central to the biology of the virus. However, direct proof of a role for the tax gene in the transformation of T cells is lacking. The events involved in subsequent progression to tumorigenesis are almost completely unknown. As with adult T-cell leukemia (ATL) and its etiologic agent HTLV-I, HTLV-II is associated with a human T-lymphocyte malignancy. Details of the mechanism of tumorigenesis are yet to be explained. Differences in the severity and prognosis of HTLV-II-associated atypical hairy-cell leukemia, compared to ATL, likely result from late (nonviral) events in the formation and outgrowth of tumor cells. (64 Refs)
Keywords: Cell Transformation, Neoplastic/GENETICS Cell Transformation, Viral *Cloning, Molecular Gene Expression Regulation, Leukemic/*PHYSIOLOGY Gene Expression Regulation, Viral/*PHYSIOLOGY Genes, pX/GENETICS Genes, Viral/GENETICS Human HTLV-II/*GENETICS Leukemia, T-Cell, HTLV-II-Associated/*MICROBIOLOGY Proviruses/GENETICS Trans-Activation (Genetics)/PHYSIOLOGY Transcription, Genetic/GENETICS Virus Replication/GENETICS MONOGRAPH REVIEW
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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.
