Fusion Inhibitors
Fusion Inhibitors - Related Videos
02:45
Assessment of Viral Fusion Inhibitors Using a Cre-Inducible Fluorescent Reporter
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2026
Source: Esposito, A. M.,et al. High-throughput Cre-Lox Activated Viral Membrane Fusion Assay to Identify Inhibitors of HIV-1 Viral Membrane Fusion. J. Vis. Exp. (2018)This video demonstrates a co-culture fluorescent assay to monitor cell-to-cell viral transmission. The assay uses a red-to-green reporter cassette to visualize viral membrane fusion and evaluate the efficacy of test compounds in blocking viral entry.
02:45
Nuclear Fusion
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2020
The process of converting very light nuclei into heavier nuclei is also accompanied by the conversion of mass into large amounts of energy, a process called fusion. The principal source of energy in the sun is a net fusion reaction in which four hydrogen nuclei fuse and ultimately produce one helium nucleus and two positrons. A helium nucleus has a mass that is 0.7% less than that of four hydrogen nuclei; this lost mass is converted into energy during the fusion. This reaction produces about...
07:22
A High-throughput Cre-Lox Activated Viral Membrane Fusion Assay to Identify Inhibitors of HIV-1 Viral Membrane Fusion
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Cited by 8 •
2018
We describe a cell-based assay to report on HIV-1 fusion via the expression of green fluorescent protein detectable by flow cytometry or fluorescence microscopy. It can be used to test inhibitors of viral entry (specifically at the fusion step) in cell-free and cell-to-cell infection systems.
09:19
Analysis of SNARE-mediated Membrane Fusion Using an Enzymatic Cell Fusion Assay
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2012
We have developed a cell fusion assay that quantifies SNARE-mediated membrane fusion events by activated expression of β-galactosidase.
01:52
Eukaryotic Transcription Inhibitors
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2020
Certain biochemical processes, such as embryonic development and cell growth regulation, depend on the repression of specific genes. DNA binding proteins known as eukaryotic transcription inhibitors regulate the repression of gene expression in eukaryotes. The presence of these inhibitors at the required location and time in the cell is triggered by the presence of hormones and additional signals from other cells. Eukaryotic transcription inhibitors usually contain two distinct domains, a DNA...
FAQs
Binding can stabilize the viral fusion protein in an inactive shape, preventing the structural changes needed to bring the viral membrane and host-cell membrane into close contact. Without that rearrangement, the membranes cannot progress toward formation of a fusion pore. This mechanism makes the viral entry protein a direct target for antiviral intervention.
Agents directed at viral fusion proteins act on the machinery that drives membrane merger, whereas agents targeting host-cell receptors block an interaction required for the virus to approach or engage the cell membrane. Both strategies interrupt entry, but they act at different points: one disables the viral protein, while the other prevents the necessary host-cell contact.
Entry inhibition acts before the virus begins replication inside the host cell. Blocking membrane fusion at this early stage can prevent the viral genome or other entry-associated components from reaching the cell interior, limiting infection at its starting point. This timing distinguishes fusion inhibition from strategies aimed at processes that occur after replication has begun.
A study can first identify whether the candidate interacts with a viral fusion protein or a host-cell receptor. Researchers then consider whether that interaction locks the viral protein in an inactive shape or blocks the close membrane contact required for a fusion pore. The resulting entry-blocking effect provides a basis for evaluating antiviral potential.
Research focuses on diseases caused by enveloped viruses because their entry can require fusion between a viral lipid membrane and a host-cell membrane. HIV and respiratory viruses are examples highlighted in this context. Studying these systems supports targeted treatment strategies that act during entry, before viral replication becomes established in the cell.
Fusion-inhibitor research helps clarify how membrane fusion is regulated, including the roles of protein shape, receptor engagement, and membrane proximity. These principles extend beyond viral entry because certain cellular events also require lipid membranes to merge. Consequently, the topic connects antiviral drug design with broader questions about membrane behavior in biology.