@article {10.3844/ajidsp.2008.69.75, article_type = {journal}, title = {Patient and Mouse Antibodies against Dengue Virus Nonstructural Protein 1 Cross-React with Platelets and Cause Their Dysfunction or Depletion}, author = {Lin, Chiou-Feng and Lei, Huan-Yao and Liu, Ching-Chuan and Liu, Hsiao-Sheng and Yeh, Trai-Ming and Anderson, Robert and Lin, Yee-Shin}, volume = {4}, number = {1}, year = {2008}, month = {Mar}, pages = {69-75}, doi = {10.3844/ajidsp.2008.69.75}, url = {https://thescipub.com/abstract/ajidsp.2008.69.75}, 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.}, journal = {American Journal of Infectious Diseases}, publisher = {Science Publications} }