2017年，斯里兰卡遭受了最严重的登革热流行并报告了高发病率下的严重和异常表现。此次爆发与登革病毒-2（DENV-2）的重新出现有关，其负责株被确定为先前流行的DENV-2世界性基因型的变异。本研究对此次流行中患者的DENV-2世界性基因型进行了表征。此外，我们还确定了对感染该病毒的患者登革热感染严重程度产生影响的宿主因素。我们随机选择了康迪国家医院的91例患者的急性血清样本。其中，40.2％和48.9％分别为登革热IgM阳性和IgG阳性。NS1抗原水平在初次感染中明显较高。严重登革热（SD）和伴告警征的登革热（DWWS）组的病毒基因组和感染力滴度明显高于不伴告警征的登革热（DWoWS）组。SD患者的病毒血症水平最高。至于宿主细胞因子反应，DWoWS组的干扰素α（IFN-α）水平显著高于DWWS组和SD组，而SD患者的白细胞介素（IL）-12p40和肿瘤坏死因子α（TNF-α）水平显著高于其他两组。TNF-α、IL-4和单核细胞趋化蛋白-1浓度与NS1抗原水平呈正相关。通过全基因组分析，NS4具有最高频率的氨基酸变异，其次是E基因。我们的研究表明，病毒血症水平和免疫反应对SD结果产生影响，并且这些发现可能有助于确定针对SD感染的有效治疗策略。

In 2017, Sri Lanka experienced its largest dengue epidemic and reported severe and unusual presentations of dengue with high morbidity. This outbreak was associated with the reemergence of dengue virus-2 (DENV-2), with the responsible strain identified as a variant of the previously circulating DENV-2 cosmopolitan genotype. In this study, we characterized the DENV-2 cosmopolitan genotype from patients during this epidemic. Also, we identified host factors that contributed to the severity of dengue infection in patients infected with this particular virus. Ninety-one acute serum samples from patients at the National Hospital in Kandy were randomly selected. Of these, 40.2% and 48.9% were positive for dengue IgM and IgG, respectively. NS1 antigen levels were significantly higher in primary infections. The severe dengue (SD) and dengue with warning signs (DWWS) groups exhibited significantly higher viral genome and infectivity titers than the dengue without warning signs (DWoWS) group. The highest viremia level was observed in SD patients. As for host cytokine response, interferon α (IFN-α) levels were significantly higher in the DWoWS group than in the DWWS and SD groups, whereas interleukin (IL)-12p40 and tumor necrosis factor α (TNF-α) levels in SD patients were significantly higher than in the other two groups. The TNF-α, IL-4, and monocyte chemoattractant protein-1 concentrations were positively correlated with NS1 antigen levels. From whole-genome analysis, NS4 had the highest frequency of amino acid variants, followed by the E gene. Our study suggests that viremia levels and immune responses contributed to SD outcomes, and these findings may help in identifying an effective therapeutic strategy against SD infection.