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

Research output: Contribution to journalArticle

12 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)69-75
Number of pages7
JournalAmerican Journal of Infectious Diseases
Volume4
Issue number1
Publication statusPublished - 2008
Externally publishedYes

Keywords

  • Autoantibody
  • Dengue virus
  • NS1
  • Platelet

ASJC Scopus subject areas

  • Infectious Diseases

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