A recent study investigating the acute and early convalescent B cell response in dengue patients has found dengue virus to have a significant B cell activation capacity, causing a transient but high appearance of plasmablast and plasma cell, coinciding with that of dengue-specific IgG antibodies at day 4-7 after onset of fever [37] . The similarity of D29 Fab-IgG to germline sequence suggests that such antibodies are present in the immune repertoire of naïve individuals and given the inherent high affinity of D29, such antibodies may be preferentially selected during clonal expansion and maintained as memory. Indeed, antibodies that cross-react between prM and E has been isolated from memory B cells in primary and secondary dengue patients [9, 11] . The original immunogens for these cross-reactive antibodies are difficult to determine since they were generated in the course of natural infections, but it would be interesting to identify the epitope and germline of these antibodies and compare the sequences with D29 Fab-IgG. and prM, 10 mg/ml of synthetic peptides corresponding to prM (A) and E (B) was incubated with D29 Fab-IgG. Peptides corresponding to E were tested individually but presented as groups of 5. For all experiments, 2610 6 pfu/ml of DENV2 or imDENV2 was included as control antigen. M1-32: 15 mer peptides corresponding to prM. Pr1-5: .20 mer custom-made peptides covering parts of prM. E1-73: 15 mer peptides corresponding to E. (**p-value,0.005) (TIF)  Lack of Association between CLEC5A Gene Single-Nucleotide Polymorphisms and Kawasaki Disease in Taiwanese Children Background. Kawasaki disease is characterized by systemic vasculitis of unknown etiology. Previous genetic studies have identified certain candidate genes associated with susceptibility to KD and coronary artery lesions. Host innate immune response factors are involved in modulating the disease outcome. The aim of this study was to investigate CLEC5A (C-type lectin domain family 5) genetic polymorphisms with regards to the susceptibility and outcome of KD. Methods. A total of 1045 subjects (381 KD patients and 664 controls) were enrolled to identify 4 tagging single-nucleotide polymorphisms (tSNPs) of CLEC5A (rs1285968, rs11770855, rs1285935, rs1285933) by using the TaqMan Allelic Discrimination Assay. The Hardy-Weinberg equilibrium was assessed in cases and controls, and genetic effects were evaluated by the chi-square test. Results. No significant associations were noted between the genotypes and allele frequency of the 4 CLEC5A tSNPs between controls and patients. In the patients, polymorphisms of CLEC5A showed no significant association with coronary artery lesion formation and intravenous immunoglobulin treatment response. Conclusions. This study showed for the first time that polymorphisms of CLEC5A are not associated with susceptibility to KD, coronary artery lesion formation, and intravenous immunoglobulin treatment response in a Taiwanese population. Kawasaki disease (KD) is characterized by acute, febrile, and systemic vasculitis and was first described by Kawasaki et al. in 1974 [1] . In developed countries, KD is the leading cause of acquired heart diseases in children [2, 3] . KD occurs worldwide and particularly in Japan, Korea, and Taiwan and mainly affects children less than 5 years of age [4] [5] [6] . The most serious complication of KD is the occurrence of coronary artery lesions (CALs) [7, 8] . The prevalence of KD in children younger than 5 years is the highest in Japan, followed by Korea and Taiwan, and lowest in Europe. Previous studies have either failed to identify causative pathogens for KD or reported discrepant results [9] [10] [11] . Therefore, it is possible that a genetic background plays an important role in the pathogenesis of KD.