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

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12 Citations (Scopus)


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
Issue number1
Publication statusPublished - 2008
Externally publishedYes



  • Autoantibody
  • Dengue virus
  • NS1
  • Platelet

ASJC Scopus subject areas

  • Infectious Diseases

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