TY - JOUR
T1 - Antibody-dependent enhancement of heterotypic dengue infections involved in suppression of IFNγ production
AU - Yang, Kuender D.
AU - Yeh, Wen Ting
AU - Yang, Ming Yu
AU - Chen, Rong Fu
AU - Shaio, Men Fang
PY - 2001
Y1 - 2001
N2 - 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 IFNγ 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 × 104 vs. 2.8 ± 0.3 × 102 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 IFNγ production (56 ± 24 vs. 12 ±3 pg/ml). The addition of IFNγ (0.1 μg/ml) suppressed significantly the antibody-dependent enhancement induced by dengue-1 immune sera, whereas the presence of anti-IFNγ 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.
AB - 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 IFNγ 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 × 104 vs. 2.8 ± 0.3 × 102 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 IFNγ production (56 ± 24 vs. 12 ±3 pg/ml). The addition of IFNγ (0.1 μg/ml) suppressed significantly the antibody-dependent enhancement induced by dengue-1 immune sera, whereas the presence of anti-IFNγ 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.
KW - Antibody-dependent enhancement
KW - Dengue hemorrhagic fever
KW - Plaque-forming units (PFU)
KW - T cell helper 1 (Th1) response
UR - http://www.scopus.com/inward/record.url?scp=0035129304&partnerID=8YFLogxK
U2 - 10.1002/1096-9071(20000201)63:2<150::AID-JMV1010>3.0.CO;2-A
DO - 10.1002/1096-9071(20000201)63:2<150::AID-JMV1010>3.0.CO;2-A
M3 - 文章
C2 - 11170052
AN - SCOPUS:0035129304
SN - 0146-6615
VL - 63
SP - 150
EP - 157
JO - Journal of Medical Virology
JF - Journal of Medical Virology
IS - 2
ER -
