Disease relevance of bel-1

• The transcriptional transactivator of human foamy virus maps to the bel 1 genomic region [1].
• The Bel-1 protein of human foamy virus activates human immunodeficiency virus type 1 gene expression via a novel DNA target site [2].
• The regulation mechanism of HFV bel1 protein-mediated transactivation appears to be analogous to that of some DNA virus transactivators that increase transcription from numerous different viral promoters with little sequence similarity shared among them [3].
• The bel1 protein of human foamy virus (HFV), a retrovirus, regulates expression of the gene linked to the HFV long terminal repeat (LTR) and is essential for viral gene expression [3].
• The Bel-1 protein of human foamy virus can activate transcription directed by the long terminal repeat (LTR) promoter of human immunodeficiency virus type 1 (HIV-1) [2].

High impact information on bel-1

• A construct expressing bel 1 under control of a heterologous promoter was found to transactivate the HFV long terminal repeat in a dose-dependent fashion [1].
• The role of the bel 1 genomic region as a transactivator was further investigated by eukaryotic expression of a genome fragment of HFV spanning the bel 1 open reading frame [1].
• Results presented here confirmed this and showed further that a deletion introduced only into the bel 1 open reading frame of a plasmid derived from an infectious molecular clone of HFV abolished transactivation [1].
• The bel1 protein transactivates HFV long terminal repeat (LTR)-directed gene expression by recognizing a region in U3 [4].
• To dissect the role of individual promoters and bel genes on transgene expression and neurotoxicity we generated transgenic mice with a construct termed pL-bel1, which lacks the IP and the ancillary genes except bel-1 [5].

References