Abstract
Dengue virus infection elicits a spectrum of clinical presentations ranging from asymptomatic to severe disease. The mechanisms leading to severe dengue are not known, however it has been reported that the complement system is hyper-activated in severe dengue. Screening of complement proteins demonstrated that C1q, a pattern recognition molecule, can bind directly to dengue virus envelope protein and to whole dengue virus serotype 2. Incubation of dengue virus serotype 2 with C1q prior to infection of THP-1 cells led to decreased virus infectivity and modulation of mRNA expression of immunoregulatory molecules suggesting reduced inflammatory responses.
Keywords:
C1q; Classical complement pathway; Dengue; Dengue fever; Dengue hemorrhagic fever; Viral persistence.
Copyright © 2013 Elsevier B.V. All rights reserved.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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B7-2 Antigen / genetics
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B7-2 Antigen / immunology
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Cell Adhesion Molecules / genetics
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Cell Adhesion Molecules / immunology
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Cell Line
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Complement C1q / immunology
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Complement C1q / metabolism*
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Dengue / genetics*
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Dengue / immunology
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Dengue / metabolism
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Dengue / virology
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Dengue Virus / classification
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Dengue Virus / immunology
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Dengue Virus / physiology*
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Humans
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Inflammation Mediators / immunology*
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Lectins, C-Type / genetics
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Lectins, C-Type / immunology
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Lipopolysaccharide Receptors / genetics
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Lipopolysaccharide Receptors / immunology
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Protein Binding
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Receptors, Cell Surface / genetics
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Receptors, Cell Surface / immunology
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Viral Envelope Proteins / genetics
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Viral Envelope Proteins / metabolism
Substances
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B7-2 Antigen
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Cell Adhesion Molecules
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DC-specific ICAM-3 grabbing nonintegrin
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Inflammation Mediators
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Lectins, C-Type
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Lipopolysaccharide Receptors
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Receptors, Cell Surface
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Viral Envelope Proteins
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Complement C1q