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Updated: May 3, 2026

Dissecting Host-virus Interaction in Lytic Replication of a Model Herpesvirus
Published on: October 7, 2011
Sphingosine kinase 1 regulates measles virus replication
Madhuvanthi Vijayan1, Young-Jin Seo1, Curtis John Pritzl1
1Departments of Surgery & Molecular Microbiology and Immunology, University of Missouri-Columbia, Columbia, MO 65212, USA.
Abstract:
Measles virus (MV) manipulates host factors to facilitate virus replication. Sphingosine kinase (SK) is an enzyme catalyzing the formation of sphingosine 1-phosphate and modulates multiple cellular processes including the host defense system. Here, we determined the role of SK1 in MV replication. Overexpression of SK1 enhanced MV replication. In contrast, inhibition of SK impaired viral protein expression and infectious virus production from cells expressing MV receptor, SLAM or Nectin-4. The inhibition of virus replication was observed when the cells were infected by vaccine strain or wild type MV or V/C gene-deficient MV. Importantly, SK inhibition suppressed MV-induced activation of NF-κB. The inhibitors specific to NF-κB signal pathway repressed the synthesis of MV proteins, revealing the importance of NF-κB activation for efficient MV replication. Therefore, SK inhibition restricts MV replication and modulates the NF-κB signal pathway, demonstrating that SK is a cellular factor critical for MV replication.
Insights
Sphingosine kinase (SK) inhibition restricts measles virus (MV) replication by impacting viral protein synthesis. This study reveals SK as a critical host factor essential for efficient MV propagation and NF-κB pathway activation.
Area of Science:
- Virology
- Cell Biology
- Biochemistry
Background:
- Measles virus (MV) relies on host factors for replication.
- Sphingosine kinase (SK) regulates cellular processes, including host defense.
Purpose of the Study:
- To investigate the role of Sphingosine Kinase 1 (SK1) in measles virus replication.
- To determine if SK inhibition affects MV propagation and associated signaling pathways.
Main Methods:
- Overexpression and inhibition of SK1 in cells expressing MV receptors (SLAM, Nectin-4).
- Assessed viral protein expression and infectious virus production.
- Investigated the impact of SK inhibition on NF-κB signaling pathway activation.
Main Results:
- SK1 overexpression enhanced MV replication.
- SK inhibition impaired viral protein expression and infectious virus production across different MV strains.
- SK inhibition suppressed MV-induced NF-κB activation.
- NF-κB pathway inhibition also repressed MV protein synthesis.
Conclusions:
- Sphingosine kinase (SK) is a crucial host factor for efficient measles virus replication.
- SK inhibition restricts MV replication, partly by modulating the NF-κB signaling pathway.
- Targeting SK represents a potential strategy for antiviral therapies against measles.
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