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Imaging of HIV-1 Envelope-induced Virological Synapse and Signaling on Synthetic Lipid Bilayers
Published on: March 8, 2012
CD4+ lipid bilayers. A model for human immunodeficiency virus type 1 coat protein binding
M T Tosteson1, P F Tosi, C Nicolau
1Department of Cellular and Molecular Physiology, Harvard Medical School, Boston, Massachusetts 02115.
The Journal of Biological Chemistry
|June 25, 1991
Summary
The human immunodeficiency virus type 1 (HIV-1) gp120 protein forms ion channels upon binding to CD4 receptors. This interaction is blocked by MHCII or OKT4A, suggesting a new method for detecting gp120.
Area of Science:
- Virology
- Immunology
- Biophysics
Background:
- The human immunodeficiency virus type 1 (HIV-1) coat glycoprotein, gp120, binds to the CD4 molecule on T-lymphocytes.
- CD4 also serves as a receptor for major histocompatibility complex class II (MHCII).
Purpose of the Study:
- To investigate the molecular events following the interaction between HIV-1 gp120 and CD4.
- To develop a method for detecting gp120 using CD4-incorporated lipid bilayers.
Main Methods:
- Incorporation of CD4 into lipid bilayers.
- Recording electrical changes upon addition of gp120 to CD4-containing bilayers.
- Assessing the effect of MHCII and OKT4A antibody pre-exposure on channel formation.
Main Results:
- Interaction of gp120 with CD4-containing bilayers induced multistate ion-permeable channels.
- Maximum channel conductance was measured at 380-400 picosiemens.
- Pre-exposure of CD4+ bilayers to MHCII or OKT4A antibody prevented channel formation upon gp120 addition.
Conclusions:
- CD4-containing bilayers bind gp120, MHCII, and OKT4A.
- Binding of gp120 to CD4 induces the formation of ion-permeable channels.
- CD4+ bilayers can be utilized as an assay for detecting gp120 in solution.
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