Source:http://linkedlifedata.com/resource/pubmed/id/11170052
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
2001-2-22
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pubmed:abstractText |
Antibody-dependent enhancement has been implicated in some outbreaks of epidemic dengue hemorrhagic fever, however, the mechanism of antibody-dependent enhancement is not well known. This study was conducted to investigate the cross-protection and cross-enhancement of dengue-2 virus infections by dengue-1 immune sera. It was found that dengue-1 immune sera at 1:5 dilution (n = 12) could neutralize dengue-2 infections in BHK-21 cells, as assessed by a standard plaque-reduction neutralization assay. Two-thirds of the dengue-1 immune sera at 1:25 dilution demonstrated neutralizing effects for dengue-2 infections, whereas, non-immune sera revealed no neutralization for dengue-2 infections in BHK-21 cells. Human mononuclear leukocytes in response to dengue-2 infections elicited a T cell helper 1 (Th1) response revealing induction of IFNgamma but not IL-4 production. Dengue-1 immune sera did not neutralize dengue-2 infections in mononuclear leukocytes. Subneutralizing titers of dengue-1 immune sera at 1:250, but not at 1:10 dilution, enhanced dengue-2 infections in mononuclear leukocytes (1.2 +/- 0.7 x 10(4) vs. 2.8 +/- 0.3 x 10(2) PFU/ml). The enhancement of dengue-2 infections in mononuclear leukocytes by dengue-1 immune sera at 1:250 was associated with an increase in the lymphocyte proliferation index, and a decrease in IFNgamma production (56 +/- 24 vs. 12 +/- 3 pg/ml). The addition of IFNgamma (0.1 microg/ml) suppressed significantly the antibody-dependent enhancement induced by dengue-1 immune sera, whereas the presence of anti-IFNgamma F(ab)2 antibody augmented the antibody-dependent enhancement effect. Results from this study suggest that suppression of Th1 response may be involved in the antibody-dependent enhancement of heterotypic dengue infections. Better regulation of Th1/Th2 reactions may be useful for prevention of heterotypic immune enhancement of dengue infections.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0146-6615
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pubmed:author | |
pubmed:copyrightInfo |
Copyright 2001 Wiley-Liss, Inc.
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pubmed:issnType |
Print
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pubmed:volume |
63
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
150-7
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:11170052-Antibodies, Viral,
pubmed-meshheading:11170052-Cell Line,
pubmed-meshheading:11170052-Cross Reactions,
pubmed-meshheading:11170052-Dengue,
pubmed-meshheading:11170052-Dengue Virus,
pubmed-meshheading:11170052-Dose-Response Relationship, Immunologic,
pubmed-meshheading:11170052-Humans,
pubmed-meshheading:11170052-Immune Sera,
pubmed-meshheading:11170052-Interferon-gamma,
pubmed-meshheading:11170052-Interleukin-10,
pubmed-meshheading:11170052-Leukocytes, Mononuclear,
pubmed-meshheading:11170052-Lymphocyte Activation,
pubmed-meshheading:11170052-Neutralization Tests,
pubmed-meshheading:11170052-Th1 Cells,
pubmed-meshheading:11170052-Viral Plaque Assay,
pubmed-meshheading:11170052-Virus Replication
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pubmed:year |
2001
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pubmed:articleTitle |
Antibody-dependent enhancement of heterotypic dengue infections involved in suppression of IFNgamma production.
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pubmed:affiliation |
Chang Gung Children's Hospital at Kaohsiung, Chang Gung University, Kaohsiung, Taiwan. yangkd@adm.cgmh.com.tw
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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