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Dissecting Host-virus Interaction in Lytic Replication of a Model Herpesvirus
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Function of Host Protein Staufen1 in Rabies Virus Replication
Gaowen Liu1, Congjie Chen1, Ruixian Xu1
1Research Center of Molecular Medicine of Yunnan Province, Faculty of Life Science and Technology, Kunming University of Science and Technology, Kunming 650500, China.
Viruses
|August 28, 2021
Summary
The host factor Staufen1 (STAU1) inhibits rabies virus (RABV) replication in neuronal cells. Down-regulating STAU1 increases viral titers and Negri body formation, suggesting STAU1 as a potential therapeutic target.
Area of Science:
- Virology
- Molecular Biology
- Cell Biology
Background:
- Rabies virus (RABV) is a lethal neurotropic virus causing significant public health issues.
- Staufen1 (STAU1), a double-stranded RNA-binding protein, is implicated in RNA virus replication, but its role in RABV infection is unknown.
Purpose of the Study:
- To investigate the role of host factor STAU1 in RABV infection.
- To elucidate the mechanism of STAU1 action during RABV infection in SH-SY-5Y cells.
Main Methods:
- Immunofluorescence and confocal microscopy to assess STAU1 and viral protein localization.
- TCID50 assays to quantify viral titers.
- Quantitative real-time PCR and Western blotting to measure viral gene and protein expression.
- RNA interference and vector transfection to modulate STAU1 expression.
Main Results:
- STAU1 colocalized with RABV nucleoprotein (N) in infected cells.
- Down-regulation of STAU1 significantly increased viral replication and titers (10-fold increase).
- Reduced STAU1 expression led to increased Negri body-like structures and viral mRNA accumulation.
Conclusions:
- STAU1 acts as an inhibitor of RABV replication in vitro.
- STAU1 is a crucial host factor influencing RABV infection dynamics.
- Findings provide insights into RABV replication mechanisms and potential therapeutic targets.
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