Activation of the human immunodeficiency virus type 2 enhancer is dependent on purine box and kappa B regulatory elements.

摘要: Abstract Human immunodeficiency virus type 2 (HIV-2) displays several features which distinguish it from HIV-1. Among the differences in these two viruses are responses of their enhancer regions to T-cell activation. For example, stimulation HIV-1 transcription is largely dependent on kappa B regulatory elements. In contrast, HIV-2 has a single site and contains additional cis-acting sequences responsive induction. One sites, previously termed CD3R, purine-rich site, also called PuB1, CD3 component receptor complex binds Elf-1, member ets proto-oncogene family. this report, we examine interaction PuB1 with other sites enhancer. We demonstrate that confers responsiveness activators only cooperation Induction at least elements addition B. another (PuB2), recombinant Elf-1. An adjacent region, proximal PuB2 (pets) shows protection DNase footprinting experiments extracts Jurkat T cells. Mutation either B, PuB2, or pets significantly reduces response stimulation, an effect mediated RNA level. Therefore, activation four elements, one found HIV-1, act synergy another. Despite sequence similarity, organization function have diverged considerably those