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Related Experiment Video

Updated: Sep 13, 2025

Generation, Amplification, and Titration of Recombinant Respiratory Syncytial Viruses

Generation, Amplification, and Titration of Recombinant Respiratory Syncytial Viruses

Published on: April 4, 2019

Host RhoA Signaling Controls Filamentous vs. Spherical Morphogenesis and Cell-to-Cell Spread of RSV via Lipid Raft

Manoj K Pastey¹, Lewis H McCurdy², Barney S Graham³

¹Department of Veterinary Biomedical Sciences, Oregon State University, Corvallis, OR 97330, USA.

|July 30, 2025

Summary

Respiratory syncytial virus (RSV) filamentous forms are linked to increased spread. Inhibiting RhoA with Rhosin reduces filamentation by disrupting lipid raft organization, offering a potential antiviral strategy.

Keywords:

RhoA Rhosin lipid raft respiratory syncytial virus

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An In vitro Model to Study Immune Responses of Human Peripheral Blood Mononuclear Cells to Human Respiratory Syncytial Virus Infection

An In vitro Model to Study Immune Responses of Human Peripheral Blood Mononuclear Cells to Human Respiratory Syncytial Virus Infection

Published on: December 10, 2013

Area of Science:

Virology
Cell Biology
Biochemistry

Background:

Respiratory syncytial virus (RSV) is a significant respiratory pathogen, especially in vulnerable populations.
RSV exhibits spherical and filamentous forms; filamentous morphology enhances infectivity and cell-to-cell spread.

Purpose of the Study:

To investigate the role of RhoA, a GTPase regulating cytoskeleton, in filamentous RSV morphogenesis.
To evaluate the efficacy of Rhosin, a selective RhoA inhibitor, in altering RSV morphology and spread.

Main Methods:

Utilized Rhosin to inhibit RhoA activity in RSV-infected cells.
Employed scanning electron microscopy, β-galactosidase-based fusion assays, and sucrose gradient velocity sedimentation.
Investigated RSV fusion (F) protein and lipid raft interactions using immunofluorescence microscopy.

Main Results:

Rhosin treatment significantly reduced filamentous RSV virion formation and cell-to-cell fusion.
Inhibition of RhoA disrupted RSV F protein colocalization with lipid rafts.
Morphological analysis showed a shift towards spherical RSV forms upon RhoA inhibition.

Conclusions:

Host RhoA signaling is crucial for filamentous RSV assembly via lipid raft organization.
Targeting RhoA with inhibitors like Rhosin offers a potential host-directed antiviral approach.
Altering RSV structural phenotypes may limit viral pathogenesis.