Galectin-9 plasma levels reflect adverse hematological and immunological features in acute dengue virus infection
Abstract
Background: Dengue virus (DENV) infection remains a major public health burden worldwide. Soluble mediators may play a critical role in the pathogenesis of acute DENV infection. Galectin-9 (Gal-9) is a soluble β-galactoside-binding lectin, with multiple immunoregulatory and inflammatory properties. Objective: To investigate plasma Gal-9 levels as a biomarker for DENV infection. Study design: We enrolled 65 DENV infected patients during the 2010 epidemic in the Philippines and measured their plasma Gal-9 and cytokine/chemokine levels, DENV genotypes, and copy number during the critical and recovery phases of illness. Results: During the critical phase, Gal-9 levels were significantly higher in DENV infected patients compared to healthy or those with non-dengue febrile illness. The highest Gal-9 levels were observed in dengue hemorrhagic fever (DHF) patients (DHF: 2464. pg/ml; dengue fever patients (DF): 1407. pg/ml; non-dengue febrile illness: 616. pg/ml; healthy: 196. pg/ml). In the recovery phase, Gal-9 levels significantly declined from peak levels in DF and DHF patients. Gal-9 levels tracked viral load, and were associated with multiple cytokines and chemokines (IL-1α, IL-8, IP-10, and VEGF), including monocyte frequencies and hematologic variables of coagulation. Further discriminant analyses showed that eotaxin, Gal-9, IFN-α2, and MCP-1 could detect 92% of DHF and 79.3% of DF, specifically (P < 0.01). Conclusion: Gal-9 appears to track DENV inflammatory responses, and therefore, it could serve as an important novel biomarker of acute DENV infection and disease severity.
Journal of Clinical Virology, 58(4), pp.635-640; 2013
Journal
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- Journal of Clinical Virology
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Journal of Clinical Virology 58 (4), 635-640, 2013-12
Elsevier
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Details 詳細情報について
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- CRID
- 1050287297251962240
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- NII Article ID
- 120006986004
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- ISSN
- 13866532
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- HANDLE
- 10069/34046
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- Text Lang
- en
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- Article Type
- journal article
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- Data Source
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- IRDB
- CiNii Articles