Important note: Information in this article was accurate in 1989. The state of the art may have changed since the publication date.
MOLECULAR BIOLOGY OF THE HTLV FAMILY
AIDS: Modern Concepts and Therapeutic Challenges. Broder S, ed. New York, Marcel Dekker, p. 39-52, 1987.. Unique Identifier : AIDSLINE ICDB/89650437 Wong-Staal F; Lab. of Tumor Cell Biology, NCI, Bethesda, MD
Abstract:
Genetic aspects of human T-lymphotropic virus (HTLV) are reviewed as they relate to infection of human hosts. Topics include genetic structures of HTLV-I, -II, and -III; assembling the genes for transactivation; transcriptional regulation of cellular genes by HTLV-I and -II leading to immortality; viral and cellular factors in HTLV-III cytopathicity; development of immunodiagnostic reagents for AIDS using recombinant DNA technology; and genetic polymorphism of HTLV-III and the prospects for a vaccine. HTLV-I, -II, and -III are the prototypes of a new category of retroviruses linked together not only by their common target cell tropism, but by a novel regulatory mechanism for virus expression that depends on transactivation by a viral protein (tat). Specific interaction between the tat protein and tat-responsive sequences in the long terminal repeat of these viruses leads to 2-3 logs increase in gene expression. The implications of this finding are manifold. Identification of a protein that is critical for viral expression provides yet another handle to limit replication of these viruses. This very efficient gene expression system can be used for overproduction of any protein desired. There is evidence that the tat genes of HTLV-I and -II are the critical transforming genes of these viruses and that they may directly activate expression of cellular genes involved in T-cell production. That cellular genes can respond to the tat proteins also implies that the strategy of transactivation may be used by the cell to turn on genes at specific stages of differentiation and/or development. Two genes of HTLV-III are of unknown function. It is possible that one of the HTLV-III-specific genes is involved in a negative regulatory mechanism, thus representing the basis of the latency of this virus. The author's studies on the genomic diversity of HTLV-III indicate that, although the envelope glycoprotein is highly variable overall, there are conserved regions that may contribute antigenic sites that are group-specific. (44 Refs)
Keywords: Acquired Immunodeficiency Syndrome/DIAGNOSIS/GENETICS/PREVENTION & CONTROL Cell Transformation, Viral Cloning, Molecular Cytopathogenic Effect, Viral Genes, Viral Human HIV/*GENETICS HTLV-I/*GENETICS HTLV-II/*GENETICS Polymorphism, Restriction Fragment Length Transcription, Genetic Viral Vaccines/ADMINISTRATION & DOSAGE MONOGRAPH REVIEW REVIEW, TUTORIAL
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Important note: Information in this article was accurate in 1989. The state of the art may have changed since the publication date.
