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Imaging of HIV-1 Envelope-induced Virological Synapse and Signaling on Synthetic Lipid Bilayers
Published on: March 8, 2012
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HIV virions sense plasma membrane heterogeneity for cell entry
Sung-Tae Yang1,2, Alex J B Kreutzberger1,2, Volker Kiessling1,2
1Center for Membrane and Cell Physiology, University of Virginia, Charlottesville, VA 22908, USA.
Science Advances
|August 8, 2017
Summary
Human immunodeficiency virus (HIV) uses cholesterol-rich cell membrane boundaries for entry, not the cholesterol-rich regions themselves. This finding clarifies the role of membrane domains in viral fusion and cell entry.
Area of Science:
- Virology
- Cell Biology
- Biophysics
Background:
- Cholesterol's role in host cell membrane fusion for human immunodeficiency virus (HIV) entry is proposed but not fully understood.
- The preference of HIV virions for cholesterol-rich heterogeneous membranes over uniformly fluid membranes for fusion remains unclear.
Purpose of the Study:
- To investigate the specific roles of cholesterol and lipid domains in HIV cell entry.
- To determine the precise locations of HIV receptors CD4 and CCR5 within heterogeneous cell membranes.
- To elucidate the mechanism of HIV membrane fusion in relation to lipid domain organization.
Main Methods:
- Utilized giant plasma membrane vesicles with distinct cholesterol-rich ordered and cholesterol-poor fluid lipid domains.
- Analyzed the localization of HIV receptors CD4 and CCR5 within these lipid domains.
- Observed and characterized the site of HIV membrane fusion relative to lipid domain boundaries.
Main Results:
- HIV receptor CD4 was found sequestered in ordered lipid domains.
- HIV co-receptor CCR5 preferentially localized at the boundaries between ordered and disordered lipid domains.
- HIV fusion occurred at the boundaries of ordered/disordered lipid domains, not within ordered regions.
Conclusions:
- Ordered/disordered lipid domain coexistence is essential for HIV fusion, though not for initial attachment.
- HIV virions appear to detect and utilize membrane discontinuities at domain boundaries for cellular entry.
- This study reveals critical insights into how cholesterol and membrane heterogeneity facilitate HIV and potentially other enveloped virus entry.
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