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Related Concept Videos

SNAREs and Membrane Fusion01:43

SNAREs and Membrane Fusion

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Once a transport vesicle has recognized its target organelle, the vesicular membrane needs to fuse with the target membrane to unload the cargo. Transmembrane proteins called SNAREs present on organelle membranes and their vesicles, mediate vesicle fusion.
SNAREs exist in pairs that symmetrically interact and catalyze the fusion of the lipid bilayers in vesicle and target organelle. v-SNARE in the vesicle membrane are single polypeptide chains that bind to a complementary t-SNARE, composed of 2...
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Fusion of Secretory Vesicles with the Plasma Membrane01:26

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Proteins and neurotransmitters in secretory vesicles can be released from a cell upon vesicle docking, priming, and fusion with the plasma membrane. Vesicles are docked and primed in preparation for the quick exocytosis of their contents in response to a stimulus. The fusion process is mainly carried out by a SNAP Receptor or SNARE complex, consisting of synaptobrevin, syntaxin-1, and SNAP-25.
In 1993, Jim Rothman proposed that the antiparallel pairing of vesicular and transmembrane SNAREs, or...
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Vesicular Tubular Clusters01:45

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After budding out from the ER membrane, some COPII vesicles lose their coat and fuse with one another to form larger vesicles and interconnected tubules called vesicular tubular clusters or VTCs. These clusters constitute a compartment at the ER-Golgi interface known as ERGIC (Endoplasmic Reticulum Golgi Intermediate Compartment). The ERGIC is a mobile membrane-bound cargo transport system that sorts proteins secreted from ER and delivers them to the Golgi.
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Viral Recombination00:57

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Cells are sometimes infected by more than one virus at once. When two viruses disassemble to expose their genomes for replication in the same cell, similar regions of their genomes can pair together and exchange sequences in a process called recombination. Alternatively, viruses with segmented genomes can swap segments in a process called reassortment.
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Fluid Mosaic Model01:19

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Scientists identified the plasma membrane in the 1890s and its principal chemical components (lipids and proteins) by 1915. The model for plasma membrane structure, proposed in 1935 by Hugh Davson and James Danielli, was the first model to be widely accepted in the scientific community. The model was based on the plasma membrane's "railroad track" appearance in early electron micrographs. Davson and Danielli theorized that the plasma membrane's structure resembled a sandwich...
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A cell's plasma membrane demarcates the cell's borders and determines the nature of its interaction with the environment. Cells exclude certain substances, take in others, and excrete some others in controlled quantities. The plasma membrane must be flexible to allow certain cells, such as red and white blood cells, to change their shape while passing through narrow capillaries. These are the more obvious plasma membrane functions. In addition, the plasma membrane's surface carries...
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A Prefusion Form of Herpes Simplex Virus 1 gB has a Distinct Antigenic Signature.

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Updated: Mar 2, 2026

Method for Measurement of Viral Fusion Kinetics at the Single Particle Level
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Herpes simplex virus Membrane Fusion.

Darin J Weed1, Anthony V Nicola2

  • 1Department of Veterinary Microbiology and Pathology, College of Veterinary Medicine, Washington State University, Pullman, WA, 99164, USA.

Advances in Anatomy, Embryology, and Cell Biology
|May 22, 2017
PubMed
Summary
This summary is machine-generated.

Herpes simplex virus (HSV) uses distinct fusion events for entry, assembly, and spread. Key viral proteins like gB, gD, and gH/gL orchestrate these essential fusion mechanisms.

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Area of Science:

  • Virology
  • Cell Biology
  • Molecular Biology

Background:

  • Herpes simplex virus (HSV) infection involves multiple fusion events critical for its lifecycle.
  • These include viral entry into host cells, de-envelopment during assembly, and cell-to-cell spread via syncytium formation.

Purpose of the Study:

  • To analyze the distinct fusion processes mediated by HSV.
  • To understand the requirements, mechanisms, and regulation of these fusion events.
  • To identify the viral proteins and host factors involved.

Main Methods:

  • Review and analysis of known HSV fusion mechanisms.
  • Consideration of experimental assays like transient cell-cell fusion and fusion from without.

Main Results:

  • HSV mediates at least five distinct fusion events: entry (endocytic or plasma membrane), de-envelopment, and syncytium formation.
  • These processes rely on a combination of viral proteins and host cell factors.
  • The core viral machinery, including glycoprotein B (gB), glycoprotein D (gD), and the glycoprotein H/glycoprotein L (gH/gL) heterodimer, is crucial for most HSV fusion.

Conclusions:

  • HSV employs a complex and regulated fusion strategy involving multiple viral proteins.
  • Understanding these fusion mechanisms is key to comprehending HSV pathogenesis and developing antiviral therapies.