Chau Tran Nguyen Bich, Quyen Nguyen Than Ha, Thuy Tran Thi, Tuan Nguyen Minh, Hoang Dang Minh, Dung Nguyen Thi Phuong, Lien Le Bich, Quy Nguyen Thien, Hieu Nguyen Trong, Hieu Lu Thi Minh, Hien Tran Tinh, Hung Nguyen Thanh, Farrar Jeremy, Simmons Cameron P
Oxford University Clinical Research Unit, Hospital for Tropical Diseases, Ho Chi Minh City, Vietnam.
J Infect Dis. 2008 Aug 15;198(4):516-24. doi: 10.1086/590117.
The pathogenesis of severe dengue is not well understood. Maternally derived subneutralizing levels of dengue virus-reactive IgG are postulated to be a critical risk factor for severe dengue during infancy. In this study, we found that, in healthy Vietnamese infants, there was a strong temporal association between the Fc-dependent, dengue virus infection-enhancing activity of neat plasma and the age-related epidemiology of severe dengue. We then postulated that disease severity in infants with primary infections would be associated with a robust immune response, possibly as a consequence of higher viral burdens in vivo. Accordingly, in infants hospitalized with acute dengue, the activation phenotype of peripheral-blood NK cells and CD8+ and CD4+ T cells correlated with overall disease severity, but HLA-A*1101-restricted NS3(133-142)-specific CD8+ T cells were not measurable until early convalescence. Plasma levels of cytokines/chemokines were generally higher in infants with dengue shock syndrome. Collectively, these data support a model of dengue pathogenesis in infants whereby antibody-dependent enhancement of infection explains the age-related case epidemiology and could account for antigen-driven immune activation and its association with disease severity. These results also highlight potential risks in the use of live attenuated dengue vaccines in infants in countries where dengue is endemic.
严重登革热的发病机制尚未完全明确。母源的登革病毒反应性IgG亚中和水平被认为是婴儿期严重登革热的关键危险因素。在本研究中,我们发现,在健康的越南婴儿中,纯血浆的Fc依赖性登革病毒感染增强活性与严重登革热的年龄相关流行病学之间存在强烈的时间关联。然后我们推测,原发性感染婴儿的疾病严重程度可能与强大的免疫反应有关,这可能是体内病毒载量较高的结果。因此,在因急性登革热住院的婴儿中,外周血NK细胞、CD8⁺和CD4⁺T细胞的活化表型与总体疾病严重程度相关,但直到恢复期早期才能检测到HLA-A*1101限制性NS3(133-142)特异性CD8⁺T细胞。登革热休克综合征婴儿的血浆细胞因子/趋化因子水平通常较高。总体而言,这些数据支持婴儿登革热发病机制的一种模型,即抗体依赖性感染增强解释了与年龄相关的病例流行病学,并可能导致抗原驱动的免疫激活及其与疾病严重程度的关联。这些结果还凸显了在登革热流行国家对婴儿使用减毒活登革热疫苗的潜在风险。