Important note: Information in this article was accurate in 1990. The state of the art may have changed since the publication date.
STUDIES ON TRANSACTIVATION BY HUMAN T CELL LEUKEMIA VIRUS
Diss Abstr Int [B]; 50(9):3846 1990. Unique Identifier : AIDSLINE ICDB/90665700 Kitado H; Univ. of California, Irvine
Abstract:
We have inserted sequences from the human T-cell leukemia viruses (HTLVs) that are responsive to tax, into the long terminal repeats (LTRs) of Moloney murine leukemia virus (M-MuLV). The inserted HTLV sequences conferred tax-response to the Moloney promoter in transient expression assays whether or not the Moloney enhancers were also present in the LTR. Infectious recombinant M-MuLVs containing chimeric LTRs were also generated, and found to be responsive to tax in infectivity. These recombinant M-MuLVs, which contained tax-responsive sequences from the HTLV-II LTR in addition to, or in substitution for the Moloney enhancers, were infected into both NIH-3T3 cell line and a tax-producing NIH-3T3 cell line (15S-5a), and the chromatin structures of the proviruses were analyzed by DNase I hypersensitive (HS) site mapping technique. The results indicated that tax does not change the chromatin structure. Furthermore, presence of HS sites associated with the HTLV 21 bp repeats suggested binding of cellular factors to these sequences. When cellular factors that specifically bind to the HTLV 21 bp element were examined by UV cross-linking technique, some novel factors were discovered. These increased their affinity for the 21 bp element with increasing concentration of the 21 bp element. Binding activities of several factors were found to be dependent upon the growth state of cells, and to be altered by cAMP levels. The chimeric M-MuLV that contained the tax-responsive sequences of HTLV-II within the wild type Moloney LTRs was also injected into neonatal mice, and the tumors induced were analyzed. 11 out of 12 animals had T-cell leukemias, with 6 of them showing a possibly novel type of T-cell leukemia. The results suggest that the inserted HTLV sequences may have altered the type of disease normally induced by the wild type M-MuLV. (Full text available from University Microfilms International, Ann Arbor, MI, as Order No. AAD90-05436)
Keywords: Animal Cell Line Enhancer Elements (Genetics) Gene Expression Regulation, Viral Human HTLV-BLV Viruses/*GENETICS Leukemia, Experimental/GENETICS Leukemia, T-Cell/GENETICS Mice Moloney Leukemia Virus/GENETICS Recombination, Genetic Repetitive Sequences, Nucleic Acid *Trans-Activation (Genetics) Trans-Activators/GENETICS THESIS 900930
M9094777
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Important note: Information in this article was accurate in 1990. The state of the art may have changed since the publication date.
