title: Human immunodeficiency virus type-1 envelope glycoprotein gp120 induces expression of fusion regulatory protein (FRP)-1/CD98 on CD4+ T cells: a possible regulatory mechanism of HIV-induced syncytium formation.
abstract: Syncytium formation is one of major cytopathic effects of human immunodeficiency virus (HIV) infection, and requires the interaction of CD4 molecules on uninfected cells with HIV envelope glycoprotein gp120 expressed on HIV-infected cells. Recent evidence suggests chemokine receptors function as fusion cofactors. We have recently found that fusion regulatory protein (FRP)-1/ CD98 is involved in syncytium formation of HIV gp160-expressing U2ME-7 cells and TALL-1 cells persistently infected with HIV. However, resting lymphocytes were found to express no FRP-1 molecule. In this study, we demonstrated that recombinant gp120 (rpg120) has the ability to induce expression of FRP-1 on peripheral blood mononuclear cells (PBMC). Three-color flow cytometric analysis showed that rgp120-induced FRP-1 was expressed selectively on CD4+ T cells in a dose-dependent manner. FRP-1 expression level was maximum 3 days after addition of rgp120. Anti-CD4 and anti-gp120 antibodies blocked rgp120-induced FRP-1 expression. Co-cultivation of PBMC with HIV-1 gp160-expressing HeLa cells also resulted in the increased expression of FRP-1 on T cells. These results suggest that FRP-1 molecules are induced on CD4+ T cells via CD4-gp120 interaction and may play an important role in regulation of HIV-induced syncytium formation.
authors.affiliation: Department of Microbiology, Mie University School of Medicine, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Suga
authors.forename: M
authors.initials: M
authors.lastname: Tsurudome
authors.forename: M
authors.initials: M
authors.lastname: Ito
authors.forename: S
authors.initials: S
authors.lastname: Ohgimoto
authors.forename: N
authors.initials: N
authors.lastname: Tabata
authors.forename: M
authors.initials: M
authors.lastname: Nishio
authors.forename: M
authors.initials: M
authors.lastname: Kawano
authors.forename: H
authors.initials: H
authors.lastname: Komada
authors.forename: M
authors.initials: M
authors.lastname: Ito
authors.forename: M
authors.initials: M
authors.lastname: Sakurai
authors.forename: Y
authors.initials: Y
authors.lastname: Ito
mesh_terms: D015703:Antigens, CD / Q000096:biosynthesis*; D015496:CD4-Positive T-Lymphocytes / Q000187:drug effects / Q000276:immunology / Q000473:pathology*; D002352:Carrier Proteins / Q000096:biosynthesis*; D002459:Cell Fusion; D018920:Coculture Techniques; D003208:Concanavalin A / Q000494:pharmacology; D003588:Cytopathogenic Effect, Viral; D005434:Flow Cytometry; D027261:Fusion Regulatory Protein-1; D015726:Giant Cells; D015699:HIV Envelope Protein gp120 / Q000276:immunology*; D019302:HIV Envelope Protein gp160 / Q000096:biosynthesis; D015497:HIV-1 / Q000276:immunology*; D006367:HeLa Cells; D006801:Humans; D007376:Interleukin-2 / Q000494:pharmacology; D018448:Models, Immunological
chemical_list: D015703:Antigens, CD; D002352:Carrier Proteins; D027261:Fusion Regulatory Protein-1; D015699:HIV Envelope Protein gp120; D019302:HIV Envelope Protein gp160; D007376:Interleukin-2; D003208:Concanavalin A