Human herpesvirus 7 induces the down-regulation of CD4 antigen in lymphoid T cells without affecting p56lck levels.

摘要: In this study, we investigated the fate of CD4 Ag during infection CD4+ T cells with lymphotrophic human herpesvirus 7 (HHV-7), using SupT1 lymphoblastoid cell line as a model system. The following points were established: 1) productive HHV-7 was required to obtain persistent down-modulation surface (CD4SURF); 2) at 6 9 days postinfection, when approximately 50 60% still showed CD4SURF dim positivity, drastic loss total protein found by either Western blot or immunoprecipitation experiments; 3) block in production demonstrated radioimmunoprecipitation assay; 4) analysis mRNA steady-state levels and transfection studies performed plasmid containing promoter/enhancer regions front luciferase gene indicated that has suppressive effect on transcription; 5) both intracellular (CD4INTRA) reduced HHV-7-infected respect uninfected controls, but more dramatic than CD4INTRA; 6) immunogold labeling electron microscopy CD4INTRA co-localized Ags within same subcellular compartments infected cells; 7) amount tyrosine kinase p56lck phosphorylated unchanged versus cells.