Autoantibodies and molecular mimicry represent another contributory factor in dengue disease pathogenesis. Autoantibodies against platelets [63-65], endothelial cells [66,67] and coagulatory molecules [66,68-70] have been observed in dengue patient sera and associated with severe dengue. Molecular mimicry between platelets, endothelial cells or coagulatory molecules with NS1, prM and E proteins may explain the cross-reactivity of anti-NS1, anti-prM or anti-E Abs to host proteins. The consequences arising from these cross-reactive Abs include platelet dysfunction, endothelial cell apoptosis, coagulation defect, and macrophage activation
Autoantibodies and molecular mimicry represent another contributory factor in dengue disease pathogenesis. Autoantibodies against platelets [63-65], endothelial cells [66,67] and coagulatory molecules [66,68-70] have been observed in dengue patient sera and associated with severe dengue. Molecular mimicry between platelets, endothelial cells or coagulatory molecules with NS1, prM and E proteins may explain the cross-reactivity of anti-NS1, anti-prM or anti-E Abs to host proteins. The consequences arising from these cross-reactive Abs include platelet dysfunction, endothelial cell apoptosis, coagulation defect, and macrophage activation
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