4th International AIDS Conference Stockholm, Sweden. — June 12-16, 1988

Int Conf AIDS. 1988 Jun 12-16;4:1.117 (abstract no. 1017)

J.D. Rosenblatt¹, W. Wachsman², A.J. Cann¹, D.J. Slamon¹, and I.S.Y. Chen^1
1Division of Hematology-Oncology, UCLA Department of Medicine, Los Angeles, California; ²Hematology-Oncology, UCSD School of Medicine, San Diego, California

Transcription from the viral promotor (LTR) of the human T-cell leukemia viruses type I (HTLV-I) and type II (HTLV-II) is regulated by nonstructural transacting viral genes located at the 3' end of their genomes. One gene encodes a protein (p40^xI in HTLV-I and p37^xII in HTLV II) which increases transcription from the homologous viral LTR (transactivation). An overlapping gene of unknown function (here designated as "rex" for "regulator of expression") has been identified in both HTLV-I and HTLV-II. We made recombinant constructs which express the rex gene product(s) of HTLV-II (p26^x6/p24^x6) in vitro and have verified synthesis of the rex protein(s) by radio-immunoprecipitation. We assayed for effects of rex on transactivation of the HTLV-II LTR, using a transient DNA transfection system in COS cells, and human lymphoid cell lines. Low levels of rex are necessary for optimal LTR linked expression in vitro. At low levels of expression rex acts to specifically augment transactivation. When rex mutations are introduced into infectious HTLV-II clones the resultant mutants transcribe very low levels of viral mRNA. However, as much higher rex expression levels are achieved in vitro an unexpected decrease in transactivation is observed, suggesting a possible role in establishing latent infection. These observations have implications for the regulation of other human retroviruses by transacting genes, specifically HIV.

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