Liu Ching-Chuan, Huang Kao-Jean, Lin Yee-Shin, Yeh Trai-Ming, Liu Hsiao-Sheng, Lei Huan-Yao
Department of Pediatrics, College of Medicine, National Cheng Kung University, Tainan, Taiwan, Republic of China.
J Med Virol. 2002 Oct;68(2):241-52. doi: 10.1002/jmv.10198.
The immune status after dengue virus infection was studied in dengue patients from an outbreak of serotype 3 dengue virus infection in the southern part of Taiwan during November and December 1998. Consecutive blood samples from 29 dengue patients, of whom 21 had dengue fever and 8 had dengue hemorrhagic fever/dengue shock syndrome, were collected, and the immunophenotypes of the peripheral blood mononuclear cells were determined by flow cytometry. The early activation marker CD69 appeared on lymphocytes and monocytes at day 4 after the onset of fever, and declined afterward. However, a transient reverse in the CD4/CD8 ratio occurred at days 6-10 after the onset of fever. The CD4/CD8 ratio inversion was manifested in 10 of 29 dengue patients and was encountered more frequently in dengue hemorrhagic fever/dengue shock syndrome than in dengue fever patients. Analysis of the clinical blood cell count of these 10 cases showed that increase of immature neutrophils developed at fever days 5-6, CD4(dim) or CD8(dim) monocytosis at days 6-7, and atypical lymphocytosis at days 8-10 after the onset of fever. Serum IL-6 was found at either day 7 or day 9-11. The PHA-stimulated T-cell response was depressed as well. These changes in immune parameters indicate aberrant immune activation during dengue virus infection and might be involved in the pathogenesis of dengue virus infection.
1998年11月至12月，在台湾南部发生的3型登革病毒感染疫情期间，对登革热患者感染登革病毒后的免疫状态进行了研究。收集了29例登革热患者的连续血样，其中21例为登革热，8例为登革出血热/登革休克综合征，并通过流式细胞术测定外周血单个核细胞的免疫表型。发热开始后第4天，早期激活标志物CD69出现在淋巴细胞和单核细胞上，随后下降。然而，发热开始后第6至10天，CD4/CD8比值出现短暂反转。29例登革热患者中有10例出现CD4/CD8比值倒置，登革出血热/登革休克综合征患者比登革热患者更频繁出现。对这10例患者的临床血细胞计数分析显示，发热第5至6天出现未成熟中性粒细胞增多，第6至7天出现CD4（dim）或CD8（dim）单核细胞增多，发热开始后第8至10天出现非典型淋巴细胞增多。血清IL-6在第7天或第9至11天出现。PHA刺激的T细胞反应也受到抑制。这些免疫参数的变化表明登革病毒感染期间免疫激活异常，可能与登革病毒感染的发病机制有关。
