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Updated: Jul 17, 2026
09:10
siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells
Published on: October 28, 2019
Respiratory viruses activate autophagy via the IFN-STAT1/STAT5B-SOCS1 axis
Victoria Hunszinger1, Susanne Klute1, Zoé Engels1
1Institute of Molecular Virology, Ulm University Medical Center, Ulm, Germany.
Plos Pathogens
|July 15, 2026
Summary
Interferon (IFN) activates autophagy during viral infections through STAT1/STAT5B-mediated upregulation of SOCS1. This pathway is crucial for innate immunity and can be targeted to inhibit viruses that exploit autophagy.
Area of Science:
- Immunology
- Cell Biology
- Virology
Background:
- Autophagy, an ancient catabolic process, plays a role in innate immunity.
- The specific factors initiating autophagy during viral infections were previously unclear.
Purpose of the Study:
- To elucidate the mechanism by which interferons (IFNs) activate autophagy during viral infections.
- To identify key molecular players in the IFN-mediated autophagy pathway.
- To explore the therapeutic potential of targeting this pathway against autophagy-dependent viruses.
Main Methods:
- Investigated IFN-induced autophagy in cell lines and primary human lung fibroblasts.
- Utilized gene depletion and pharmacological inhibition of STAT transcription factors (STAT1, STAT5B).
- Performed transcriptome analysis to identify IFN-stimulated genes (ISGs), including SOCS1.
- Assessed the impact of modulating SOCS1 and STAT5 on viral replication (measles virus, respiratory syncytial virus).
Main Results:
- Interferons (IFN-I, II, III) activate autophagy via a JAK1-3 dependent pathway.
- Both STAT1 and STAT5B are essential for IFN-induced autophagy, associating and translocating to the nucleus upon stimulation.
- STAT5B upregulates Suppressor of Cytokine Signaling 1 (SOCS1), which is critical for IFN-induced autophagy.
- Targeting the STAT1/STAT5B-SOCS1 axis reduced virus-induced autophagy and inhibited replication of autophagy-dependent viruses (MeV, RSV).
Conclusions:
- Interferon promotes autophagy during viral infections through the STAT1/STAT5B-SOCS1 signaling axis.
- This pathway is a key component of the innate immune response to viral infections.
- Targeting this axis offers a strategy to inhibit autophagy-dependent viruses without impairing general immune defenses.
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