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08:36
Measuring Dengue Virus RNA in the Culture Supernatant of Infected Cells by Real-time Quantitative Polymerase Chain Reaction
Published on: November 1, 2018
CLEC5A is critical for dengue-virus-induced lethal disease
Szu-Ting Chen1, Yi-Ling Lin, Ming-Ting Huang
1Department and Institute of Microbiology and Immunology, National Yang-Ming University, Taipei 112, Taiwan.
Nature
|May 23, 2008
Summary
CLEC5A acts as a receptor for dengue virus (DV), triggering inflammatory cytokine release. Blocking this interaction reduces DV-induced plasma leakage and mortality in mice, offering a potential treatment for severe dengue.
Area of Science:
- Immunology
- Virology
- Molecular Biology
Background:
- Dengue hemorrhagic fever and dengue shock syndrome are severe dengue virus (DV) infections.
- These conditions involve plasma leakage and low platelet counts.
Purpose of the Study:
- To investigate the role of CLEC5A (C-type lectin domain family 5, member A) in DV infection.
- To explore CLEC5A as a potential therapeutic target for severe dengue.
Main Methods:
- Directly tested CLEC5A interaction with DV virions.
- Investigated downstream signaling pathways, including DAP12 phosphorylation and cytokine release.
- Utilized anti-CLEC5A monoclonal antibodies in mouse models of DV infection.
Main Results:
- CLEC5A directly binds DV, leading to DAP12 phosphorylation and pro-inflammatory cytokine release.
- CLEC5A-DV interaction does not mediate viral entry but stimulates cytokine production.
- Blocking CLEC5A-DV interaction suppressed cytokine release and significantly reduced DV-induced plasma leakage, hemorrhage, and mortality in STAT1-deficient mice.
Conclusions:
- CLEC5A functions as a signaling receptor for DV, mediating pro-inflammatory responses.
- Targeting the CLEC5A-DV interaction presents a promising strategy to mitigate tissue damage and improve survival in severe dengue.
- This approach may also be applicable to other virus-induced inflammatory diseases.
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