TY  - JOUR
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 
PY  - 2008
TI  - Patient and Mouse Antibodies against Dengue Virus Nonstructural Protein 1 Cross-React with Platelets and Cause Their Dysfunction or Depletion
JF  - American Journal of Infectious Diseases
VL  - 4
IS  - 1
DO  - 10.3844/ajidsp.2008.69.75
UR  - https://thescipub.com/abstract/ajidsp.2008.69.75
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.