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Updated: Mar 7, 2026

Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells
Published on: February 21, 2018
CSFV proliferation is associated with GBF1 and Rab2
Wulong Liang1, Minping Zheng, Changlei Bao
1College of Veterinary Medicine, Northwest A and F University, Yangling, Shaanxi 712100, People's Republic of China.
Abstract:
The Golgi apparatus and its resident proteins are utilized and regulated by viruses to facilitate their proliferation. In this study, we investigated Classical swine fever virus (CSFV) proliferation when the function of the Golgi was disturbed. Golgi function was disturbed using chemical inhibitors, namely, brefeldin A (BFA) and golgicide A (GCA), and RNA interfering targets, such as the Golgi-specific BFA-resistance guanine nucleotide exchange factor 1 (GBF1) and Rab2 GTPases. CSFV proliferation was significantly inhibited during RNA replication and viral particle generation after BFA and GCA treatment. CSFV multiplication dynamics were retarded in cells transfected with GBF1 and Rab2 shRNA. Furthermore, CSFV proliferation was promoted by GBF1 and Rab2 overexpression using a lentiviral system. Hence, Golgi function is important for CSFV multiplication, and GBF1 and Rab2 participate in CSFV proliferation. Further studies must investigate Golgi-resident proteins to elucidate the mechanism underlying CSFV replication.
Insights
Classical swine fever virus (CSFV) uses the Golgi apparatus for proliferation. Inhibiting Golgi function with chemicals or gene silencing significantly reduced CSFV replication, while enhancing specific Golgi proteins promoted it.
Area of Science:
- Virology
- Cell Biology
- Molecular Biology
Background:
- Viruses exploit cellular machinery, including the Golgi apparatus, for replication.
- Understanding host-pathogen interactions at the Golgi is crucial for antiviral strategies.
Purpose of the Study:
- To investigate the role of Golgi apparatus function in Classical swine fever virus (CSFV) proliferation.
- To determine the involvement of GBF1 and Rab2 GTPases in CSFV multiplication.
Main Methods:
- Disturbance of Golgi function using chemical inhibitors: brefeldin A (BFA) and golgicide A (GCA).
- Genetic manipulation of Golgi-specific proteins GBF1 and Rab2 using shRNA and lentiviral overexpression systems.
- Assessment of CSFV proliferation, RNA replication, and viral particle generation.
Main Results:
- BFA and GCA treatments significantly inhibited CSFV RNA replication and viral particle formation.
- Silencing GBF1 and Rab2 expression using shRNA retarded CSFV multiplication dynamics.
- Overexpression of GBF1 and Rab2 promoted CSFV proliferation.
Conclusions:
- Golgi apparatus function is essential for efficient CSFV multiplication.
- GBF1 and Rab2 play a significant role in supporting CSFV proliferation.
- Further research into Golgi-resident proteins is needed to fully elucidate CSFV replication mechanisms.
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