Bacterial Extracellular Vesicles (BEVs) Derived from Chryseobacterium Inhibit Dengue Virus Infection by Disrupting Its Structural Integrity

  • J Extracell Vesicles. 2026 Jun;15(6):e70302. doi: 10.1002/jev2.70302.
Yaqi Gao  1 ,  Lijian Zhang  1 ,  Tianci Zhang  1  2 ,  Qiufeng Yao  1 ,  Ruifang Gao  3 ,  Yue Wang  3 ,  Yunpeng Zhao  3 ,  Tingting Zhou  4 ,  Jikuai Chen  5 ,  Xing Zhang  5 ,  Hao Ren  1 ,  Yongzhe Zhu  1 ,  Ping Zhao  1 ,  Zhongtian Qi  1 ,  Li Luo  2 ,  Zhaoling Qin  1
Affiliations
  • 1. Department of Microbiology, Shanghai Key Laboratory of Medical Biodefense, Faculty of Naval Medicine, Naval Medical University, Shanghai, China.
  • 2. Shanghai Key Laboratory of Bio-energy Crops, Center of Plant Science, School of Life Sciences, Shanghai University, Shanghai, China.
  • 3. Department of Stem Cell and Regeneration Medicine, Translational Medicine Research Center, Naval Medical University, Shanghai, China.
  • 4. Department of Pharmaceutical Analysis, School of Pharmacy, Naval Medical University, Shanghai, China.
  • 5. Department of Health Toxicology, Faculty of Naval Medicine, Naval Medical University, Shanghai, China.
PMID: 42338006 DOI: 10.1002/jev2.70302
Abstract

Dengue Virus (DENV) Infection poses a significant global health threat, and current prevention and treatment strategies are limited by challenges of lacking effective mosquito control measures and antibody-dependent enhancement. This study reports that Bacterial extracellular vesicles (BEVs) secreted by a soil bacterium Chryseobacterium aquifrigidense M24 exhibit potent anti-DENV activity by triggering the structural disintegration of DENV particles prior to cellular entry in a dose-dependent manner. Mechanistic investigations revealed that BEVs interact with the viral envelope, inducing premature membrane fusion. This process is characterized by reduced membrane fluidity and irreversible lipid rearrangement, leading to a significant increase in particle density, as shown by iodixanol gradient ultracentrifugation. The proposed 'fusion-triggered structural disruption' is further supported by the induction of aberrant E protein oligomerization and morphological changes observed via transmission electron microscopy. This mechanism is specific to enveloped viruses, as BEVs showed no effect on non-enveloped Enterovirus 71. Crucially, this BEV-mediated inactivation extends to other enveloped viruses, including HCV, WNV and YFV, indicating broad-spectrum potential. Our findings reveal a previously unexplored function of BEVs as virucidal agents, proposing a new 'virus-destructor' strategy that contrasts with conventional fusion inhibitors and offering promising avenues for developing broad-spectrum Antiviral drugs.

Keywords
Chryseobacterium; antiviral mechanism; bacterial extracellular vesicles; dengue virus; enveloped virus.
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