Important note: Information in this article was accurate in 1992. The state of the art may have changed since the publication date.
HUMAN T-CELL LEUKEMIA VIRUS TYPE II
The Human Retroviruses. Gallo RC and Jay G, eds. San Diego, Academic Press, p. 21-33, 1991.. Unique Identifier : AIDSLINE ICDB/92678720 Chen IS; Rosenblatt JD; Dept. of Medicine, Univ. of California, Los Angeles, CA 90024
Abstract:
Since its discovery in 1982, human T-cell leukemia virus type II (HTLV-II) has been a virus for which both diseases and its origin have been sought. It is associated with rare forms of human leukemia and may be the cause of hairy cell leukemia. HTLV-II is reviewed, including discovery and epidemiology; evidence for the etiologic role of HTLV-II in chronic T-cell leukemia related to hairy cell leukemia; worldwide recognition of HTLV-II; the role of HTLV-II in human disease; in vitro biological studies of HTLV-II; the molecular genetics of HTLV-II (regulatory genes of HTLV-II, tax gene, and rex gene); and molecular mechanisms of HTLV-II-induced T-cell transformation. In general, insights gained from investigating the molecular genetics of HTLV-II have shown it to be similar to HTLV-I in terms of the overall number and arrangement of viral genes and their function in regard to viral replication. The comparative morphology of HTLV-I and HTLV-II has been extremely informative, both in highlighting important sequence and functional similarities that these viruses share, and in bringing to light differences that ultimately may be relevant to their apparently different pathogenesis. The mechanism of in vitro T-cell transformation by HTLV-II is unknown, but a number of hypotheses have emerged that parallel those proposed for HTLV-I transformation. First, it has been proposed that since the regulatory genes tax and rex are capable of regulating viral gene expression, they also may be able to regulate aberrantly cellular gene expression, resulting in immortalization of infected cells. Another hypothesis derives from observations that HTLV-I and HTLV-II can mitogenically stimulate quiescent T cells to divide in the absence of viral infection. This may involve the HTLV envelope glycoprotein and a receptor on the surface of T cells, which ordinarily may be involved in regulating normal T-cell proliferative responses. Overall, HTLV-II transformation of T cells may resemble the processes of transformation in systems involving oncogenes. Tax, and possibly Rex, and factor at the cell membrane (envelope) may act together to transduce signals, resulting in the final transformed state of T cells. (49 Refs)
Keywords: Cell Transformation, Viral/GENETICS Gene Expression Regulation, Viral/*PHYSIOLOGY Genes, pX/GENETICS/PHYSIOLOGY Human HTLV-II/*GENETICS/PATHOGENICITY HTLV-II Infections/*GENETICS/MICROBIOLOGY Leukemia, Hairy Cell/*GENETICS/MICROBIOLOGY Leukemia, T-Cell, HTLV-II-Associated/*GENETICS/MICROBIOLOGY T-Lymphocytes/MICROBIOLOGY 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.
