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Updated: Aug 14, 2025
High-throughput Antiviral Assays to Screen for Inhibitors of Zika Virus Replication
Published on: October 30, 2021
Inhibiting cardiac autophagy suppresses Zika virus replication
Xin Ma1, Yinnong Jia1, Jing Yuan1
1Yunnan Key Laboratory of Pharmacology for Natural Products, School of Pharmaceutical Science, Kunming Medical University, Kunming, China.
Insights
Zika virus (ZIKV) infection impacts the heart. This study reveals autophagy plays a key role in ZIKV infection, and inhibiting autophagy reduces viral load, offering a potential treatment strategy.
Area of Science:
- Virology
- Cell Biology
- Pathogenesis
Background:
- Zika virus (ZIKV) infection poses a global health risk, causing neurological disorders and cardiac complications.
- Effective prevention and treatment strategies are hindered by an unclear understanding of ZIKV's cardiac pathogenic mechanisms.
- The role of autophagy in ZIKV infection remains largely uninvestigated.
Purpose of the Study:
- To investigate the involvement and role of autophagy in ZIKV infection.
- To establish in vitro and in vivo models for studying ZIKV-induced cardiac pathology.
Main Methods:
- Established in vitro cardiomyocyte and in vivo mouse models of ZIKV infection.
- Monitored the expression of the autophagy protein LC3B and autophagic flux via immunofluorescence.
- Utilized autophagy inhibitors to assess their impact on ZIKV infection.
- Quantified viral copy numbers to evaluate the effect of autophagy modulation.
Main Results:
- ZIKV infection demonstrated time and concentration-dependent effects.
- LC3B levels significantly increased post-ZIKV infection, indicating autophagy activation.
- Inhibition of autophagy led to decreased LC3B levels and a reduction in viral copies.
Conclusions:
- Autophagy is actively involved in ZIKV infection.
- Inhibiting autophagy presents a promising therapeutic strategy to reduce ZIKV viral load and associated cardiac complications.
Abstract:
Zika Virus (ZIKV) infection is a global threat. Other than the congenital neurological disorders it causes, ZIKV infection has been reported to induce cardiac complications. However, the precise treatment plans are unclear. Thus, illustrating the pathogenic mechanism of ZIKV in the heart is critical to providing effective prevention and treatment of ZIKV infection. The mechanism of autophagy has been reported recently in Dengue virus infection. Whether or not autophagy participates in ZIKV infection and its role remains unrevealed. This study successfully established the in vitro cardiomyocytes and in vivo mouse models of ZIKV infection to investigate the involvement of autophagy in ZIKV infection. The results showed that ZIKV infection is both time and gradient-dependent. The key autophagy protein, LC3B, increased remarkably after ZIKV infection. Meanwhile, autophagic flux was detected by immunofluorescence. Applying autophagy inhibitors decreased the LC3B levels. Furthermore, the number of viral copies was quantified to evaluate the influence of autophagy during infection. We found that autophagy was actively involved in the ZIKV infection and the inhibition of autophagy could effectively reduce the viral copies, suggesting a potential intervention strategy for reducing ZIKV infection and the undesired complications caused by ZIKV.
