Transcription factor AP1 modulates the internal promoter activity of bovine foamy virus.

Foamy virus contains two promoters, which are the canonical long terminal repeat (LTR) promoter and the internal promoter (IP). FV gene expression was considered to initiate at the internal promoter. However, little was known about how basal transcription of IP was triggered by the host cellular factors. Previous studies found some cellular proteins could affect HFV viral replication, but it was no known whether the AP1 signal pathway was involved in the activation of viral replication or not. In this study, we reported that treatment with TPA or AP1 increased basal transcription of IP and did not affect basal transcription of the promoter in the LTR. In addition, the c-Jun mutant blocked the IP activity stimulated by TPA. Two AP1 binding sites located in BFV-IP promoter were found by bioinformatics and mutants of two AP1 binding sites decreased luciferase reporter activity of IP activated by AP1. EMSA assay showed that two AP1 binding sites could bind to c-Jun/c-Fos heterodimeric. We also found TPA and AP1 enhanced BFV3026 replication. Taken together, these data suggested that AP1 was a positive regulator of BFV internal promoter.