Human foamy virus infection activates class I major histocompatibility complex antigen expression

We examined the effect of human foamy virus (HFV) infection on the expression of human major histocompatibility complex molecules. Our data show that in vitro HFV infection of U373-MG glioblastoma cells results in increased expression of class I human leukocyte antigen (HLA) and transcripts. Transient transfection assays of plasmids containing the reporter gene chloramphenicol acetyl transferase driven by different 5' deletions of the HLA-A11 class I promoter allowed identification of cis-acting elements involved in this regulation. HFV infection has two opposite effects on the HLA class I promoter: transactivation of the HLA-A11 promoter through a positive regulatory element located in the -525 to -335 region upstream of exon 1 and down-regulation of transcriptional activity driven by the -335 to -205 class I promoter region. Additional experimental data indicate that the effect of HFV on HLA class I expression is not mediated by the interferon pathway.