Wang S, He R, Patarapotikul J, Innis B L, Anderson R
Department of Microbiology and Immunology, Dalhousie University, Halifax, Nova Scotia, Canada.
Virology. 1995 Oct 20;213(1):254-7. doi: 10.1006/viro.1995.1567.
The mechanisms underlying severe thrombocytopenia in dengue hemorrhagic fever/dengue shock syndrome (DHF/DSS) are not completely understood. We present here the first evidence that dengue type 2 virus binds to human platelets only in the presence of virus-specific antibody, supporting a role for immune-mediated clearance of platelets in the pathogenesis of thrombocytopenia in DHF/DSS. Antibody-enhanced binding of virus of platelets was also demonstrated with a panel of eight murine monoclonal antibodies specific for the dengue E protein. The degree of binding was dependent on the antibody used but not on the antibody IgG subclass, indicating that factors other than the platelet Fc receptor are involved in binding of virus-antibody complexes to the platelet surface. Confirmation that antibody-dependent virus binding to platelets is not primarily mediated by the platelet Fc receptor was obtained by demonstrating good binding even when platelets were pretreated with the Fc gamma RII-specific antibody IV.3.
登革出血热/登革休克综合征（DHF/DSS）中严重血小板减少的潜在机制尚未完全明确。我们在此首次证明，仅在存在病毒特异性抗体的情况下，登革2型病毒才会与人血小板结合，这支持了免疫介导的血小板清除在DHF/DSS血小板减少发病机制中的作用。用一组针对登革E蛋白的八种鼠单克隆抗体也证实了抗体增强的病毒与血小板的结合。结合程度取决于所用抗体，而不取决于抗体IgG亚类，这表明除血小板Fc受体外的其他因素参与了病毒-抗体复合物与血小板表面的结合。通过证明即使血小板用FcγRII特异性抗体IV.3预处理后仍有良好的结合，证实了抗体依赖性病毒与血小板的结合并非主要由血小板Fc受体介导。
