Abstract
HIV causes a chronic infection by evading immune eradication. A key element of HIV immune escape is the HIV-1 Nef protein. Nef causes a reduction in the level of cell surface major histocompatibility complex class I (MHC-I) protein expression, thus protecting HIV-infected cells from anti-HIV cytotoxic T lymphocyte (CTL) recognition and killing. Nef also reduces cell surface levels of the HIV receptor, CD4, by accelerating endocytosis. We show here that endocytosis is not required for Nef-mediated downmodulation of MHC-I molecules. The main effect of Nef is to block transport of MHC-I molecules to the cell surface, leading to accumulation in intracellular organelles. Furthermore, the effect of Nef on MHC-I molecules (but not on CD4) requires phosphoinositide 3-kinase (PI 3-kinase) activity. We propose that Nef diverts MHC-1 proteins into a PI 3-kinase-dependent transport pathway that prevents expression on the cell surface.
Copyright 2001 Academic Press.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Blotting, Western
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CD4 Antigens / metabolism
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Cell Membrane / metabolism*
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Chromones / pharmacology
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Down-Regulation
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Dynamins
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Endocytosis
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Flow Cytometry
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GTP Phosphohydrolases / metabolism
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Gene Products, nef / chemistry
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Gene Products, nef / metabolism*
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Golgi Apparatus / chemistry
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Golgi Apparatus / metabolism
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HIV-1 / physiology*
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HLA-A2 Antigen / genetics
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HLA-A2 Antigen / metabolism*
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Humans
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Morpholines / pharmacology
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Phosphatidylinositol 3-Kinases / metabolism*
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Phosphoinositide-3 Kinase Inhibitors
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Protein Transport
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Recombinant Fusion Proteins / metabolism
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Tumor Cells, Cultured
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nef Gene Products, Human Immunodeficiency Virus
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src Homology Domains
Substances
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CD4 Antigens
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Chromones
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Gene Products, nef
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HLA-A2 Antigen
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Morpholines
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Phosphoinositide-3 Kinase Inhibitors
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Recombinant Fusion Proteins
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nef Gene Products, Human Immunodeficiency Virus
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2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one
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GTP Phosphohydrolases
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Dynamins