Abstract:
The discovery of T-cell growth factor (TCGF) made possible the study of T-cells and the subsequent isolation of human T-cell leukemia lymphoma virus (HTLV), the first retrovirus unequivocally associated with a human neoplasia. A subpopulation of normal peripheral blood T-lymphocytes produces TCGF for a short time following lectin or antigen stimulations; some continuous T-cell lines produce TCGF constitutively or after stimulation. Although the leukemic TCGF appears different from normal TCGF in some biochemical properties, recent hybridization studies of cDNA obtained from both normal and neoplastic cells indicate that the abnormalities are due to post-translational modifications. With one exception, all isolates of HTLV are called HTLV-I and are closely related as determined by immunological methods and restriction enzyme analysis of integrated provirus; the exception, called HTLV-II, was isolated from a cell line established from a patient with 'hairy cell' leukemia. To study the molecular biology of the HTLV-I, the authors first cloned a defective HTLV-I provirus and then, using this clone as a probe, cloned several complete HTLV-I provirus genomes; by use of low stringency hybridization, the authors were also able to isolate sequences of the HTLV-II. Molecular and seroepidemiological studies demonstrated the presence of HTLV nucleic acid sequences or related proteins in serum specimens from all over the world; most of the people containing integrated viruses also carried HTLV-specific antibodies. HTLV-I infection is typically found in patients with characteristic clinical features including frequent skin involvement, visceral organ enlargement, lymphadenopathy, and frequent hypercalcemia. Infectivity of the virus appears to be low, and intimate, prolonged contact is required. It is not uncommon to find a pocket of seropositivity within a family where one of the members is known to have the disease. Several different mechanisms of modification of cellular onc gene expression are postulated. Insertion of promoter or enhancer sequences close to the gene, as in the insertion of viral promoter in the vicinity of a cellular onc gene is one possibility. Another possible mechanism is gene amplification. Yet another mechanism is chromosomal rearrangement, with linkage of an active promoter with an onc gene. The authors have concluded that understanding of mechanisms of viral and nonviral transformation can give an overview of normal cell differentiation and regulation as well as important insights for studying the control of neoplastic growth. (44 Refs)
Keywords: Gene Amplification Human HTLV-BLV Viruses Leukemia/ETIOLOGY/*GENETICS Lymphoma/ETIOLOGY/*GENETICS *Oncogenes *Retroviridae Infections JOURNAL ARTICLE
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