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Published on: June 26, 2019
XPO1-dependent nuclear export regulates NS3 localization and promotes DENV-2 replication through mitochondrial
Selvin Noé Palacios-Rápalo1, Jonathan Hernández-Castillo1, Luis Adrián De Jesús-González2
1Department of Infectomics and Molecular Pathogenesis, Center for Research and Advanced Studies (CINVESTAV), Mexico City, Mexico.
Nucleus (Austin, Tex.)
|July 28, 2026
Summary
Inhibiting exportin 1 (XPO1) causes dengue virus protein accumulation in the nucleus and mitochondria, enhancing viral replication by suppressing antiviral responses.
Area of Science:
- Virology
- Cell Biology
- Molecular Biology
Background:
- Nucleocytoplasmic transport is vital for cell function and exploited by viruses.
- The role of nuclear export in dengue virus (DENV) NS3 protein localization and viral replication is unclear.
Purpose of the Study:
- To investigate the role of exportin 1 (XPO1)-mediated nuclear export in DENV-2 NS3 protein localization.
- To determine the impact of XPO1 inhibition on DENV-2 replication and host antiviral responses.
Main Methods:
- Pharmacological inhibition of XPO1 in DENV-2 infected Huh-7 cells.
- Analysis of DENV-2 NS3 protein localization (nucleus, mitochondria).
- Assessment of mitochondrial morphology and type I interferon production.
Main Results:
- XPO1 inhibition led to DENV-2 NS3 accumulation in the nucleus and mitochondria.
- Mitochondrial morphology changes were observed upon XPO1 inhibition.
- Blocking nuclear export enhanced DENV-2 replication in interferon-stimulated cells by reducing type I interferon production.
Conclusions:
- XPO1-mediated nuclear export regulates DENV-2 NS3 localization.
- Nuclear export blockade links to mitochondrial remodeling and suppressed antiviral signaling during DENV infection.
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