Kurane Ichiro, Matsutani Takaji, Suzuki Ryuji, Takasaki Tomohiko, Kalayanarooj Siripen, Green Sharone, Rothman Alan L, Ennis Francis A
National Institute of Infectious Diseases, Japan.
Trop Med Health. 2011 Dec;39(4 Suppl):45-51. doi: 10.2149/tmh.2011-S09. Epub 2011 Dec 1.
Dengue virus (DENV) is a leading cause of morbidity and mortality in most tropical and subtropical areas of the world. Dengue virus infection induces specific CD4+CD8- and CD8+CD4- T cells in humans. In primary infection, T-cell responses to DENV are serotype cross-reactive, but the highest response is to the serotype that caused the infection. The epitopes recognized by DENV-specific T cells are located in most of the structural and non-structural proteins, but NS3 is the protein that is most dominantly recognized. In patients with dengue hemorrhagic fever (DHF) caused by secondary DENV infection, T cells are highly activated in vivo. These highly activated T cells are DENV-specific and oligoclonal. Multiple kinds of lymphokines are produced by the activated T cells, and it has been hypothesized that these lymphokines are responsible for induction of plasma leakage, one of the most characteristic features of DHF. Thus, T-cells play important roles in the pathogenesis of DHF and in the recovery from DENV infection.
登革病毒（DENV）是世界上大多数热带和亚热带地区发病和死亡的主要原因。登革病毒感染可诱导人体产生特异性的CD4 + CD8 - 和CD8 + CD4 - T细胞。在初次感染时，T细胞对登革病毒的反应具有血清型交叉反应性，但最高反应是针对引起感染的血清型。登革病毒特异性T细胞识别的表位位于大多数结构蛋白和非结构蛋白中，但NS3是最主要被识别的蛋白。在由二次登革病毒感染引起的登革出血热（DHF）患者中，T细胞在体内高度活化。这些高度活化的T细胞是登革病毒特异性的且为寡克隆性。活化的T细胞产生多种淋巴因子，据推测这些淋巴因子是导致血浆渗漏的原因，而血浆渗漏是登革出血热最典型的特征之一。因此，T细胞在登革出血热的发病机制以及从登革病毒感染中恢复的过程中发挥着重要作用。
