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09:10
siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells
Published on: October 28, 2019
Cytosolic DNA-induced CGAS-STING1-dependent autophagy promotes SFTSV and EV-71 replication
Xiao-Lan Gu1,2, Qiao Liu2, Wen-Kang Zhang2
1Department of Clinical Laboratory, Gansu Provincial Hospital, Lanzhou, China.
Autophagy
|July 23, 2026
Summary
Severe fever with thrombocytopenia syndrome virus (SFTSV) hijacks host autophagy for replication by activating the CGAS-STING1 pathway with mitochondrial DNA. This study reveals a novel viral strategy and potential therapeutic target.
Area of Science:
- Innate immunity and viral pathogenesis
- Cellular autophagy and host-pathogen interactions
Background:
- The cyclic GMP-AMP synthase (CGAS)-stimulator of interferon response cGAMP interactor 1 (STING1) pathway detects cytosolic DNA to initiate innate immune responses.
- While CGAS-STING1 signaling can induce autophagy, its role in RNA virus infection remains largely unknown.
- Severe fever with thrombocytopenia syndrome virus (SFTSV) is an emerging RNA virus with significant public health implications.
Purpose of the Study:
- To investigate the activation and role of CGAS-STING1-dependent autophagy during RNA virus infection.
- To elucidate the mechanism by which SFTSV exploits this pathway for its replication.
Main Methods:
- Stimulation of CGAS-STING1-dependent autophagy using cytosolic DNA transfection.
- Infection of cells with SFTSV and enterovirus 71 (EV-71) to assess viral replication.
- Analysis of mitochondrial damage and mitochondrial DNA (mtDNA) release during SFTSV infection.
- Investigation of the interaction between SFTSV nucleoprotein (NP) and STING1.
- Depletion of mtDNA to evaluate its role in SFTSV-induced autophagy and replication.
Main Results:
- Cytosolic DNA potently induces CGAS-STING1-dependent autophagy.
- Pre-activation of the CGAS-STING1 pathway enhances SFTSV and EV-71 replication.
- SFTSV infection causes mitochondrial damage, leading to mtDNA leakage into the cytoplasm.
- This endogenous mtDNA activates CGAS-STING1-dependent autophagy, which SFTSV utilizes for replication.
- SFTSV NP directly interacts with STING1, hijacking membranes for viral replication platforms.
- mtDNA depletion abrogates SFTSV-induced autophagy and impairs viral replication.
Conclusions:
- SFTSV exploits CGAS-STING1-dependent autophagy, induced by leaked mtDNA, for its replication.
- SFTSV NP directly interacts with STING1 to hijack cellular membranes for viral replication.
- This study uncovers a novel host anti-RNA virus strategy and a viral mechanism for subversion.
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