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Updated: Mar 28, 2026

siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells
Published on: October 28, 2019
Autophagy postpones apoptotic cell death in PRRSV infection through Bad-Beclin1 interaction
Ao Zhou1, Shuaifeng Li1, Faheem Ahmed Khan1
1a Key Lab of Agricultural Animal Genetics; Breeding and Reproduction of Ministry of Education; Huazhong Agricultural University ; Wuhan , China.
Abstract:
Autophagy and apoptosis play significant roles in PRRSV infection and replication. However, the interaction between these 2 processes in PRRSV replication is still far from been completely understood. In our studies, the exposure of MARC-145 cells to PRRSV confirmed the activation of autophagy and subsequent induction of apoptosis. The inhibition of autophagy by 3-methyladenine (3-MA) caused a significant increase in PRRSV-induced apoptosis, showing a potential connection between both mechanisms. Moreover, we observed an increase in Bad expression (a pro-apoptotic protein) and Beclin1 (an autophagy regulator) in virus-infected cells up to 36h. Co-immunoprecipitation assays showed the formation of Bad and Beclin1 complex in PRRSV infected cells. Accordingly, Bad co-localized with Beclin1 in MARC-145 infected cells. Knockdown of Beclin1 significantly decreased PRRSV replication and PRRSV-induced autophagy, while Bad silencing resulted in increased autophagy and enhanced viral replication. Furthermore, PRRSV infection phosphorylated Bad (Ser112) to promote cellular survival. These results demonstrate that autophagy can favor PRRSV replication by postponing apoptosis through the formation of a Bad-Beclin1 complex.
Insights
Autophagy helps Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) replicate by delaying apoptosis. This occurs through a Bad-Beclin1 complex, highlighting a key interaction in PRRSV infection.
Area of Science:
- Virology
- Cellular Biology
- Immunology
Background:
- Autophagy and apoptosis are crucial in Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) infection.
- The interplay between autophagy and apoptosis during PRRSV replication remains poorly understood.
Purpose of the Study:
- To investigate the interaction between autophagy and apoptosis in MARC-145 cells during PRRSV infection.
- To elucidate the molecular mechanisms by which these processes influence viral replication.
Main Methods:
- PRRSV infection of MARC-145 cells.
- Inhibition of autophagy using 3-methyladenine (3-MA).
- Analysis of apoptosis and autophagy markers (Bad, Beclin1).
- Co-immunoprecipitation and co-localization assays.
- Gene silencing (knockdown) of Beclin1 and Bad.
- Western blot analysis for phosphorylated Bad (Ser112).
Main Results:
- PRRSV infection activated both autophagy and apoptosis in MARC-145 cells.
- Autophagy inhibition (3-MA) increased PRRSV-induced apoptosis.
- Bad and Beclin1 expression increased, forming a complex and co-localizing in infected cells.
- Beclin1 knockdown reduced viral replication and autophagy.
- Bad silencing enhanced autophagy and viral replication.
- PRRSV infection phosphorylated Bad (Ser112), promoting cell survival.
Conclusions:
- Autophagy promotes PRRSV replication by inhibiting apoptosis via a Bad-Beclin1 complex.
- Targeting the Bad-Beclin1 interaction could be a strategy to control PRRSV infection.
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