Patient and Mouse Antibodies against Dengue Virus Nonstructural Protein 1 Cross-React with Platelets and Cause Their Dysfunction or Depletion
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Published On: 31 March 2008
Copyright: © 2020 Chiou-Feng Lin, Huan-Yao Lei, Ching-Chuan Liu, Hsiao-Sheng Liu, Trai-Ming Yeh, Robert Anderson and Yee-Shin Lin. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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.
- dengue virus