Human immunodeficiency virus-1 Nef suppresses Hsp70-mediated Tat activation

The human immunodeficiency virus type 1 (HIV-1) long terminal repeat (LTR) contains binding sites for several host transcription factors that contribute to HIV-1 gene expression. Although previous reports have indicated that HIV-1 Nef positively or negatively regulates HIV-1 gene expression, the precise molecular mechanisms by which this occurs remain largely unknown. In this study, we report that Nef suppressed LTR-driven transcription only in the presence of HIV-1 Tat, which was localized to the cytoplasm and degraded by the proteasome. However, the depletion of Hsp70 was found to reduce the suppressive effect of Nef on HIV-1 gene expression. These results suggest that Nef suppresses Hsp70-mediated HIV-1 Tat activation. Structured summary of protein interactions: Tat and Nef colocalize by fluorescence microscopy (View interaction) Hsp70 physically interacts with Tat by anti tag coimmunoprecipitation (View interaction) (C) 2011 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.