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Updated: Feb 20, 2026

Paramyxoviruses for Tumor-targeted Immunomodulation: Design and Evaluation Ex Vivo
Published on: January 7, 2019
MiRNA-124 is a link between measles virus persistent infection and cell division of human neuroblastoma cells
Hila Naaman1, Glenn Rall2, Christine Matullo2
1The Shraga Segal Department of Microbiology and Immunology and Genetics, Faculty of Health Sciences Ben-Gurion University of the Negev, Beer Sheva, Israel.
Abstract:
Measles virus (MV) infects a variety of lymphoid and non-lymphoid peripheral organs. However, in rare cases, the virus can persistently infect cells within the central nervous system. Although some of the factors that allow MV to persist are known, the contribution of host cell-encoded microRNAs (miRNA) have not been described. MiRNAs are a class of noncoding RNAs transcribed from genomes of all multicellular organisms and some viruses, which regulate gene expression in a sequence-specific manner. We have studied the contribution of host cell-encoded miRNAs to the establishment of MV persistent infection in human neuroblastoma cells. Persistent MV infection was accompanied by differences in the expression profile and levels of several host cell-encoded microRNAs as compared to uninfected cells. MV persistence infection of a human neuroblastoma cell line (UKF-NB-MV), exhibit high miRNA-124 expression, and reduced expression of cyclin dependent kinase 6 (CDK6), a known target of miRNA-124, resulting in slower cell division but not cell death. By contrast, acute MV infection of UKF-NB cells did not result in increased miRNA-124 levels or CDK6 reduction. Ectopic overexpression of miRNA-124 affected cell viability only in UKF-NB-MV cells, causing cell death; implying that miRNA-124 over expression can sensitize cells to death only in the presence of MV persistent infection. To determine if miRNA-124 directly contributes to the establishment of MV persistence, UKF-NB cells overexpressing miRNA-124 were acutely infected, resulting in establishment of persistently infected colonies. We propose that miRNA-124 triggers a CDK6-dependent decrease in cell proliferation, which facilitates the establishment of MV persistence in neuroblastoma cells. To our knowledge, this is the first report to describe the role of a specific miRNA in MV persistence.
Insights
MicroRNAs (miRNAs) play a role in persistent measles virus (MV) infections in the brain. Increased miRNA-124 levels in neuroblastoma cells reduce cell division, aiding MV persistence.
Area of Science:
- Virology
- Molecular Biology
- Neuroscience
Background:
- Measles virus (MV) can cause persistent central nervous system infections.
- The role of host cell-encoded microRNAs (miRNAs) in MV persistence is unknown.
- miRNAs are key regulators of gene expression.
Purpose of the Study:
- To investigate the contribution of host cell-encoded miRNAs to persistent MV infection in human neuroblastoma cells.
- To identify specific miRNAs involved in MV persistence.
Main Methods:
- Studied miRNA expression profiles in persistently infected versus uninfected human neuroblastoma cells.
- Analyzed the expression of miRNA-124 and its target, cyclin-dependent kinase 6 (CDK6).
- Utilized ectopic miRNA-124 overexpression and acute MV infection models.
Main Results:
- Persistent MV infection correlated with altered miRNA expression, including increased miRNA-124.
- High miRNA-124 levels were associated with reduced CDK6 expression and slower cell division.
- Overexpression of miRNA-124 sensitized persistently infected cells to death and facilitated MV persistence establishment.
Conclusions:
- Host cell miRNA-124 contributes to the establishment of persistent MV infection in neuroblastoma cells.
- miRNA-124-mediated CDK6 downregulation likely facilitates MV persistence by reducing cell proliferation.
- This is the first study to report a specific miRNA's role in MV persistence.

