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Author Spotlight: Advancing Antiviral Strategies Through Novel Immunocapture and Mass Spectrometry Techniques
Published on: January 12, 2024
Characterisation of a secreted MFSD6-Fc microbody as a decoy receptor for respiratory enterovirus D68
Zhaoxue Li1, Huili Li1, Xize Liu1
1Cancer Centre, The First Hospital of Jilin University, Changchun, Jilin, 130021, China; Institute of Virology and AIDS Research, The First Hospital of Jilin University, Changchun, Jilin, 130021, China.
Background:
Enterovirus D68 (EV-D68) is a prominent non-polio enterovirus known to cause severe respiratory infections and poliomyelitis-like illnesses in children. Recently, we identified MFSD6 as a receptor for EV-D68, providing a potential target for blocking viral entry into cells. This study aimed to develop an MFSD6-based decoy receptor to neutralise EV-D68 and elucidate its mechanism of action.
Methods:
In this study, we engineered a secreted MFSD6-Fc microbody (secMFSD6 Mb) and evaluated its efficacy using in vitro binding assays (co-immunoprecipitation, RT-qPCR), electron microscopy, and functional studies in EV-D68-infected respiratory cell lines (Calu-3, BEAS-2B, A549), primary human bronchial epithelial cells (HBECs), and a neonatal ICR mouse model (n = 9 per group) infected with EV-D68. Statistical significance was determined by two-way ANOVA and t-test (GraphPad Prism 8.0.2; significance threshold P < 0.05).
Findings:
secMFSD6 Mb occupies the receptor-binding sites on the viral surface, reducing virus attachment to cells by >90% (n = 3 biological replicates). Electron microscopy showed conversion of intact virions to empty capsids after Mb treatment, and sucrose-gradient analysis demonstrated a 6-fold increase in free viral RNA (F2 fraction) compared with control. In mice challenged with 1 × 107 TCID50 of US/MO/14-18947, secMFSD6 Mb increased 15-day survival from 11% (1/9) to 89% (8/9).
Interpretation:
This decoy receptor strategy may support the development of effective therapeutic approaches against EV-D68 infection.
Funding:
HYPNSFC Excellent Young Scientist Fund (32222005), the National Natural Science Foundation of China (82372226, 82172246), the National Major Project for Infectious Disease Control and Prevention (2018ZX10731-101-001-016).
Insights
A novel decoy receptor targeting MFSD6 effectively neutralizes Enterovirus D68 (EV-D68), significantly reducing viral attachment and increasing survival rates in mice. This approach shows promise for developing new EV-D68 therapies.
Area of Science:
- Virology
- Immunology
- Drug Discovery
Background:
- Enterovirus D68 (EV-D68) causes severe respiratory illness and polio-like symptoms in children.
- MFSD6 was recently identified as a key receptor for EV-D68 entry into host cells.
- Targeting the EV-D68-MFSD6 interaction presents a potential therapeutic strategy.
Purpose of the Study:
- To engineer an MFSD6-based decoy receptor to neutralize EV-D68.
- To investigate the mechanism of action of this decoy receptor.
- To evaluate the therapeutic efficacy of the decoy receptor against EV-D68 infection.
Main Methods:
- Engineered a secreted MFSD6-Fc microbody (secMFSD6 Mb).
- Assessed binding and neutralization using in vitro assays (co-immunoprecipitation, RT-qPCR) and electron microscopy.
- Evaluated efficacy in EV-D68-infected cell lines and a neonatal mouse model.
Main Results:
- secMFSD6 Mb reduced EV-D68 attachment to cells by over 90%.
- Electron microscopy revealed conversion of intact virions to empty capsids upon treatment.
- In vivo, secMFSD6 Mb increased 15-day survival in mice from 11% to 89%.
Conclusions:
- The MFSD6-based decoy receptor effectively neutralizes EV-D68.
- This strategy demonstrates potential for developing novel therapeutics against EV-D68.
- Further development of decoy receptor strategies could combat EV-D68 infections.
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