Patient and mouse antibodies against dengue virus nonstructural protein 1 cross-react with platelets and cause their dysfunction or depletion

Chiou Feng Lin, Huan Yao Lei, Ching Chuan Liu, Hsiao Sheng Liu, Trai Ming Yeh, Robert Anderson, Yee Shin Lin

研究成果: 雜誌貢獻文章

12 引文 (Scopus)

摘要

Thrombocytopenia is a clinical manifestation in dengue virus (DV) infection, yet its pathogenic mechanisms are unresolved. We previously showed that dengue patient sera contained antibodies cross-reactive with platelets. In this study, we demonstrated that the anti-platelet activity of dengue patient sera was due to the antibodies against DV nonstructural protein 1 (NS1). Studies using DV-infected or recombinant NS1-immunized mouse sera showed that anti-NS1 antibodies cross-reacted with human platelets. The platelet-binding activity of dengue patient sera or anti-NS1 antibodies was inhibited by treatment of platelets with anti-NS1 or patient sera. Further investigation showed that anti-NS1 antibodies were able to inhibit platelet aggregation and cause platelet lysis in the presence of complement. The platelet-binding activity and the induction of platelet lysis mediated by dengue patient sera or anti-NS1 antibodies were increased when platelets were activated by ADP or thrombin. Taken together, anti-NS1 antibodies account for the cross-reactivity with platelets and cause platelet dysfunction or depletion, which may be involved in the pathogenesis of dengue diseases.

原文英語
頁(從 - 到)69-75
頁數7
期刊American Journal of Infectious Diseases
4
發行號1
出版狀態已發佈 - 2008
對外發佈Yes

指紋

Dengue Virus
Blood Platelets
Antibodies
Dengue
Proteins
Serum
Virus Diseases
Platelet Aggregation
Recombinant Proteins
Thrombin
Thrombocytopenia
Adenosine Diphosphate

ASJC Scopus subject areas

  • Infectious Diseases

引用此文

Patient and mouse antibodies against dengue virus nonstructural protein 1 cross-react with platelets and cause their dysfunction or depletion. / Lin, Chiou Feng; Lei, Huan Yao; Liu, Ching Chuan; Liu, Hsiao Sheng; Yeh, Trai Ming; Anderson, Robert; Lin, Yee Shin.

於: American Journal of Infectious Diseases, 卷 4, 編號 1, 2008, p. 69-75.

研究成果: 雜誌貢獻文章

Lin, Chiou Feng ; Lei, Huan Yao ; Liu, Ching Chuan ; Liu, Hsiao Sheng ; Yeh, Trai Ming ; Anderson, Robert ; Lin, Yee Shin. / Patient and mouse antibodies against dengue virus nonstructural protein 1 cross-react with platelets and cause their dysfunction or depletion. 於: American Journal of Infectious Diseases. 2008 ; 卷 4, 編號 1. 頁 69-75.
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abstract = "Thrombocytopenia is a clinical manifestation in dengue virus (DV) infection, yet its pathogenic mechanisms are unresolved. We previously showed that dengue patient sera contained antibodies cross-reactive with platelets. In this study, we demonstrated that the anti-platelet activity of dengue patient sera was due to the antibodies against DV nonstructural protein 1 (NS1). Studies using DV-infected or recombinant NS1-immunized mouse sera showed that anti-NS1 antibodies cross-reacted with human platelets. The platelet-binding activity of dengue patient sera or anti-NS1 antibodies was inhibited by treatment of platelets with anti-NS1 or patient sera. Further investigation showed that anti-NS1 antibodies were able to inhibit platelet aggregation and cause platelet lysis in the presence of complement. The platelet-binding activity and the induction of platelet lysis mediated by dengue patient sera or anti-NS1 antibodies were increased when platelets were activated by ADP or thrombin. Taken together, anti-NS1 antibodies account for the cross-reactivity with platelets and cause platelet dysfunction or depletion, which may be involved in the pathogenesis of dengue diseases.",
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AU - Lin, Chiou Feng

AU - Lei, Huan Yao

AU - Liu, Ching Chuan

AU - Liu, Hsiao Sheng

AU - Yeh, Trai Ming

AU - Anderson, Robert

AU - Lin, Yee Shin

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N2 - Thrombocytopenia is a clinical manifestation in dengue virus (DV) infection, yet its pathogenic mechanisms are unresolved. We previously showed that dengue patient sera contained antibodies cross-reactive with platelets. In this study, we demonstrated that the anti-platelet activity of dengue patient sera was due to the antibodies against DV nonstructural protein 1 (NS1). Studies using DV-infected or recombinant NS1-immunized mouse sera showed that anti-NS1 antibodies cross-reacted with human platelets. The platelet-binding activity of dengue patient sera or anti-NS1 antibodies was inhibited by treatment of platelets with anti-NS1 or patient sera. Further investigation showed that anti-NS1 antibodies were able to inhibit platelet aggregation and cause platelet lysis in the presence of complement. The platelet-binding activity and the induction of platelet lysis mediated by dengue patient sera or anti-NS1 antibodies were increased when platelets were activated by ADP or thrombin. Taken together, anti-NS1 antibodies account for the cross-reactivity with platelets and cause platelet dysfunction or depletion, which may be involved in the pathogenesis of dengue diseases.

AB - Thrombocytopenia is a clinical manifestation in dengue virus (DV) infection, yet its pathogenic mechanisms are unresolved. We previously showed that dengue patient sera contained antibodies cross-reactive with platelets. In this study, we demonstrated that the anti-platelet activity of dengue patient sera was due to the antibodies against DV nonstructural protein 1 (NS1). Studies using DV-infected or recombinant NS1-immunized mouse sera showed that anti-NS1 antibodies cross-reacted with human platelets. The platelet-binding activity of dengue patient sera or anti-NS1 antibodies was inhibited by treatment of platelets with anti-NS1 or patient sera. Further investigation showed that anti-NS1 antibodies were able to inhibit platelet aggregation and cause platelet lysis in the presence of complement. The platelet-binding activity and the induction of platelet lysis mediated by dengue patient sera or anti-NS1 antibodies were increased when platelets were activated by ADP or thrombin. Taken together, anti-NS1 antibodies account for the cross-reactivity with platelets and cause platelet dysfunction or depletion, which may be involved in the pathogenesis of dengue diseases.

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