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The Journal of Immunology, Vol 159, Issue 7 3412-3423, Copyright © 1997 by American Association of Immunologists
ARTICLES |
P Secchiero, D Gibellini, L Flamand, I Robuffo, M Marchisio, S Capitani, RC Gallo and G Zauli
Institute of Human Virology, University of Maryland at Baltimore 21201, USA.
In this study, we investigated the fate of the CD4 Ag during infection of CD4+ T cells with the T lymphotrophic human herpesvirus 7 (HHV-7), using the SupT1 lymphoblastoid T cell line as a model system. The following points were established: 1) productive infection with HHV-7 was required to obtain persistent down-modulation of surface CD4 (CD4SURF); 2) at 6 to 9 days postinfection, when approximately 50 to 60% of SupT1 cells still showed a CD4SURF dim positivity, a drastic loss of total CD4 protein was found by either Western blot or immunoprecipitation experiments; 3) a block in CD4 protein production was demonstrated by a radioimmunoprecipitation assay; 4) analysis of the mRNA steady-state levels and transfection studies performed with a plasmid containing the CD4 promoter/enhancer regions in front of the luciferase gene indicated that HHV-7 infection has a suppressive effect on CD4 transcription; 5) both CD4SURF and intracellular CD4 (CD4INTRA) were reduced in HHV-7-infected cells with respect to uninfected controls, but the loss of CD4SURF was more dramatic than that of CD4INTRA; 6) immunogold labeling and electron microscopy demonstrated that CD4INTRA co-localized with HHV-7 Ags within the same subcellular compartments of infected cells; and 7) the total amount of the tyrosine kinase p56lck and tyrosine phosphorylated p56lck levels were unchanged in HHV-7-infected versus uninfected cells.
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