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Updated: Jun 17, 2026
08:21
Visualization of HIV-1 Gag Binding to Giant Unilamellar Vesicle (GUV) Membranes
Published on: July 28, 2016
Human immunodeficiency virus type-1 gag and host vesicular trafficking pathways
Hin Chu1, Jaang-Jiun Wang, Paul Spearman
1Department of Pediatrics and Microbiology and Immunology, Emory University School of Medicine, Atlanta, GA 30322, USA.
Current Topics in Microbiology and Immunology
|December 17, 2009
Summary
The Human Immunodeficiency Virus type 1 (HIV-1) Gag protein utilizes cellular trafficking pathways to assemble viral particles. This review details the vesicular transport mechanisms and cellular components involved in HIV-1 assembly and budding.
Area of Science:
- Virology
- Cell Biology
- Molecular Biology
Background:
- The Human Immunodeficiency Virus type 1 (HIV-1) Gag protein is essential for viral particle assembly.
- HIV-1 assembly occurs at specific cellular locations, primarily the plasma membrane, but uniquely in macrophages within intracellular compartments.
- Understanding these trafficking pathways is crucial for developing antiviral strategies.
Purpose of the Study:
- To review the cellular vesicular trafficking pathways exploited by HIV-1 Gag.
- To identify and describe the cellular components that interact with Gag during assembly and budding.
Main Methods:
- Literature review of current research on HIV-1 assembly and cellular trafficking.
- Analysis of studies investigating the role of lipid rafts, PI(4,5)P(2), adaptor protein complexes, and motor proteins.
Main Results:
- Gag recruits components of the cellular vesicular trafficking machinery to move through the cytoplasm.
- Specific cellular compartments and molecules, including lipid rafts and PI(4,5)P(2), influence Gag's plasma membrane targeting.
- Adaptor protein complexes, sorting pathways, multivesicular bodies, and motor proteins are implicated in facilitating HIV assembly.
Conclusions:
- HIV-1 Gag hijacks sophisticated cellular vesicular trafficking systems for efficient viral assembly.
- The precise mechanisms and cellular factors governing Gag localization and assembly remain an active area of research with therapeutic implications.
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