title: Modulation of surface transferrin receptors in lymphoid cells de novo infected with human immunodeficiency virus type-1.
abstract: To investigate whether transferrin receptor (CD71) expression is affected by acute HIV-1 infection, three different lymphoid cell lines (MT-4, SUPT-1, H9) were infected with HIV-1 and tested for surface CD71 expression after different incubation periods depending on cell survival after infection. We found that expression of surface CD71 was lower in cells infected with HIV-1 than in uninfected controls: the timing and extent of this down-modulation depended apparently on the different susceptibility of the cell lines to HIV-1 infection and cytopathogenicity. Citrate, a molecule capable of chelating iron, dose-dependently prevented down-modulation of surface CD71 in HIV-1 infected cells as well as viral cytopathic effects. We conclude that (i) expression of surface transferrin receptors is down-modulated by acute HIV-1 infection in T lymphoid cells, that (ii) this cell phenotypic modulation is associated with the cytopathic effects of the virus, and that (iii) these phenomena are modulated by iron chelation. These results support the view that iron metabolism may be an important area for interaction between HIV-1 and human cells.
authors: Department of Medical and Surgical Sciences, University of Turin, Italy. asavarino@medscape.com
authors: A
authors: A
authors: Savarino
authors: L
authors: L
authors: Calosso
authors: A
authors: A
authors: Piragino
authors: C
authors: C
authors: Martini
authors: L
authors: L
authors: Gennero
authors: G P
authors: GP
authors: Pescarmona
authors: A
authors: A
authors: Pugliese
mesh_terms: D036541:ADP-ribosyl Cyclase; D051997:ADP-ribosyl Cyclase 1; D000911:Antibodies, Monoclonal; D015703:Antigens, CD / Q000032:analysis / Q000276:immunology / Q000378:metabolism; D000943:Antigens, Differentiation / Q000032:analysis / Q000276:immunology / Q000378:metabolism; D000944:Antigens, Differentiation, B-Lymphocyte / Q000032:analysis / Q000276:immunology / Q000378:metabolism; D015496:CD4-Positive T-Lymphocytes / Q000737:chemistry / Q000378:metabolism* / Q000821:virology*; D002614:Chelating Agents / Q000494:pharmacology; D002951:Citrates; D015536:Down-Regulation / Q000187:drug effects / Q000502:physiology; D005434:Flow Cytometry; D015658:HIV Infections / Q000378:metabolism*; D015497:HIV-1; D006801:Humans; D016130:Immunophenotyping; D066298:In Vitro Techniques; D007501:Iron / Q000378:metabolism; D008562:Membrane Glycoproteins; D009244:NAD+ Nucleosidase / Q000032:analysis / Q000276:immunology / Q000378:metabolism; D011990:Receptors, Transferrin / Q000032:analysis / Q000276:immunology / Q000378:metabolism*; D000077559:Sodium Citrate
chemical_list: D000911:Antibodies, Monoclonal; D015703:Antigens, CD; D000943:Antigens, Differentiation; D000944:Antigens, Differentiation, B-Lymphocyte; C068126:CD71 antigen; D002614:Chelating Agents; D002951:Citrates; D008562:Membrane Glycoproteins; D011990:Receptors, Transferrin; D000077559:Sodium Citrate; D007501:Iron; D036541:ADP-ribosyl Cyclase; C498154:CD38 protein, human; D009244:NAD+ Nucleosidase; D051997:ADP-ribosyl Cyclase 1