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Enterovirus 71 virion-associated galectin-1 facilitates viral replication and stability
Pei-Huan Lee1, Chia-Ming Liu1, Tzong-Shiann Ho2
1Department of Microbiology & Immunology, College of Medicine, National Cheng Kung University, Tainan, 701, Taiwan.
Plos One
|February 24, 2015
Summary
Galectin-1 facilitates Enterovirus 71 (EV71) infection by binding to the virus and host cells. Reducing galectin-1 levels impairs EV71 infectivity and pathogenicity, revealing a novel therapeutic target.
Area of Science:
- Virology
- Immunology
- Molecular Biology
Background:
- Enterovirus 71 (EV71) causes severe diseases, including fatal brain stem encephalitis, posing a significant threat to children's health.
- EV71 infection begins with viral attachment to host cells, influenced by cell receptors and potentially soluble factors.
- Galectin-1's role in EV71 infection has not been previously investigated.
Purpose of the Study:
- To investigate the role of galectin-1 in Enterovirus 71 (EV71) infection.
- To determine if galectin-1 influences EV71 infectivity, pathogenicity, and stability.
Main Methods:
- Measured serum galectin-1 levels in EV71-infected children.
- Assessed galectin-1 association with EV71 viral particles (VP1, VP3) in infected cells.
- Propagated EV71 in galectin-1 knockdown cells and evaluated viral infectivity, pathogenicity in mice, and stability.
Main Results:
- Serum galectin-1 levels were elevated in EV71-infected children.
- Galectin-1 associated with EV71 VP1 and VP3, facilitating viral spread to new cells.
- EV71 propagated from galectin-1 knockdown cells showed reduced infectivity, pathogenicity, and thermal/storage stability.
Conclusions:
- Galectin-1 plays a crucial role in facilitating EV71 infection.
- Galectin-1 enhances EV71 infectivity, pathogenicity, and viral stability.
- Targeting galectin-1 may offer a novel therapeutic strategy against EV71.
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