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Updated: May 10, 2026

Arbovirus Infections As Screening Tools for the Identification of Viral Immunomodulators and Host Antiviral Factors
Published on: September 13, 2018
Inhibition of multiplication of the prototypic arenavirus LCMV by valproic acid
Ángela Vázquez-Calvo1, Miguel A Martín-Acebes, Juan-Carlos Sáiz
1Centro de Biología Molecular Severo Ochoa UAM-CSIC, Cantoblanco, Madrid, Spain.
Abstract:
Valproic acid (VPA), a short chain fatty acid commonly used for treatment of neurological disorders, has been shown to inhibit production of infectious progeny of different enveloped viruses including the prototypic arenavirus lymphocytic choriomeningitis virus (LCMV). In this study we have investigated the mechanisms by which VPA inhibits LCMV multiplication in cultured cells. VPA reduced production of infectious LCMV progeny and virus propagation without exerting a major blockage on either viral RNA or protein synthesis, but rather affecting the cell release and specific infectivity of LCMV progeny from infected cells. Our results would support the repurposing of VPA as a candidate antiviral drug to combat arenavirus infections.
Insights
Valproic acid inhibits the spread of lymphocytic choriomeningitis virus (LCMV) by affecting virus release, not synthesis. This suggests repurposing valproic acid as a potential antiviral for arenavirus infections.
Area of Science:
- Virology
- Drug Repurposing
- Molecular Biology
Background:
- Valproic acid (VPA) is a anticonvulsant drug with known antiviral properties against enveloped viruses.
- Lymphocytic choriomeningitis virus (LCMV) is a prototypic arenavirus that causes significant disease.
Purpose of the Study:
- To investigate the mechanism by which VPA inhibits LCMV multiplication in cell cultures.
- To evaluate VPA as a potential antiviral agent against arenavirus infections.
Main Methods:
- Cell culture experiments were performed to assess LCMV replication.
- Viral RNA and protein synthesis were measured.
- Virus release and infectivity were analyzed.
Main Results:
- VPA treatment reduced infectious LCMV progeny and virus propagation.
- VPA did not significantly inhibit viral RNA or protein synthesis.
- VPA affected the release and specific infectivity of LCMV from infected cells.
Conclusions:
- VPA's antiviral effect on LCMV is mediated by influencing virus release and infectivity.
- VPA shows promise as a candidate antiviral drug for treating arenavirus infections.
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