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HIV-1 Nef Binds a Subpopulation of MHC-I throughout Its Trafficking Itinerary and Down-regulates MHC-I by Perturbing Both Anterograde and Retrograde Trafficking

The HIV protein Nef is thought to mediate immune evasion and promote viral persistence in part by down-regulating major histocompatibility complex class I protein (MHC-I or HLA-I) from the cell surface. Two different models have been proposed to explain this phenomenon as follows: 1) stimulation of...

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Published in:The Journal of biological chemistry 2010-10, Vol.285 (40), p.30884-30905
Main Authors: Yi, Ling, Rosales, Tilman, Rose, Jeremy J., Chaudhury, Bhabhadeb, Knutson, Jay R., Venkatesan, Sundararajan
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description The HIV protein Nef is thought to mediate immune evasion and promote viral persistence in part by down-regulating major histocompatibility complex class I protein (MHC-I or HLA-I) from the cell surface. Two different models have been proposed to explain this phenomenon as follows: 1) stimulation of MHC-I retrograde trafficking from and aberrant recycling to the plasma membrane, and 2) inhibition of anterograde trafficking of newly synthesized HLA-I from the endoplasmic reticulum to the plasma membrane. We show here that Nef simultaneously uses both mechanisms to down-regulate HLA-I in peripheral blood mononuclear cells or HeLa cells. Consistent with this, we found by using fluorescence correlation spectroscopy that a third of diffusing HLA-I at the endoplasmic reticulum, Golgi/trans-Golgi network, and the plasma membrane (PM) was associated with Nef. The binding of Nef was similarly avid for native HLA-I and recombinant HLA-I A2 at the PM. Nef binding to HLA-I at the PM was sensitive to specific inhibition of endocytosis. It was also attenuated by cyclodextrin disruption of PM lipid micro-domain architecture, a change that also retarded lateral diffusion and induced large clusters of HLA-I. In all, our data support a model for Nef down-regulation of HLA-I that involves both major trafficking itineraries and persistent protein-protein interactions throughout the cell.
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source ScienceDirect®; PubMed Central
subjects Adapter Proteins
Anterograde transport
Cell Biology
Cell Membrane - genetics
Cell Membrane - metabolism
Cell surface
Cell Surface Receptor
cyclodextrin
Data processing
Endocytosis
Endocytosis - genetics
Endoplasmic reticulum
Endoplasmic Reticulum - genetics
Endoplasmic Reticulum - metabolism
FCS
fluorescence spectroscopy
FRAP
Golgi apparatus
Golgi Apparatus - genetics
Golgi Apparatus - metabolism
HeLa Cells
Histocompatibility
Histocompatibility antigen HLA
Histocompatibility Antigens Class I - genetics
Histocompatibility Antigens Class I - metabolism
HIV-1 - genetics
HIV-1 - metabolism
Human Immunodeficiency Virus
Human immunodeficiency virus 1
Humans
Immunology
Lateral diffusion
Leukocytes, Mononuclear - metabolism
Leukocytes, Mononuclear - virology
Lipids
Major histocompatibility complex
Models, Biological
nef Gene Products, Human Immunodeficiency Virus - genetics
nef Gene Products, Human Immunodeficiency Virus - metabolism
Nef protein
Peripheral blood mononuclear cells
Plasma membranes
Protein interaction
Protein Sorting
Protein Transport
Recycling
Retrograde transport
title HIV-1 Nef Binds a Subpopulation of MHC-I throughout Its Trafficking Itinerary and Down-regulates MHC-I by Perturbing Both Anterograde and Retrograde Trafficking
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