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siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells
Published on: October 28, 2019
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Autophagy induction regulates influenza virus replication in a time-dependent manner
Neda Feizi1, Parvaneh Mehrbod1, Bizhan Romani2,3
1Influenza and Other Respiratory Viruses Department, Pasteur Institute of Iran, Tehran, Iran.
Journal of Medical Microbiology
|May 3, 2017
Summary
Inducing autophagy therapeutically inhibits influenza virus replication, while prophylactic induction can enhance it. This suggests autophagy manipulation is a promising antiviral strategy and for virus production.
Area of Science:
- Cell Biology
- Virology
- Immunology
Background:
- Autophagy is crucial for host defense against pathogens.
- Viruses, including influenza virus (IV), can manipulate autophagy for their own replication.
- IV blocks lysosome fusion, leading to autophagosome accumulation, presenting an opportunity for antiviral intervention.
Purpose of the Study:
- To investigate the impact of autophagy modulation on influenza virus replication.
- To explore the potential of targeting autophagy as an antiviral strategy.
Main Methods:
- Two cell lines were transfected with Beclin-1 expression plasmid, either before (prophylactic) or after (therapeutic) IV inoculation.
- Autophagy induction was confirmed, reaching 26% in Beclin-1 overexpressing cells.
- Viral titers (haemagglutinin and TCID50) were measured at 24 and 48 hours post-infection.
- The effect of autophagy inhibition using 3-methyladenine was also assessed.
Main Results:
- Prophylactic Beclin-1 overexpression enhanced viral titer at 24 hours post-infection but not at 48 hours.
- Therapeutic autophagy induction significantly inhibited viral replication at both 24 and 48 hours post-infection.
- Inhibition of autophagy with 3-methyladenine reduced viral replication.
Conclusions:
- Autophagy induction can control influenza virus (H1N1) titers in a time-dependent manner.
- Modulating autophagy during the viral life cycle offers dual potential for antiviral therapies and enhancing viral yield for production.
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