L Jiang1, H Guo, D Fang. 1. Department of Microbiology, Sun Yat-sen University of Medical Sciences, Guangzhou, 510089.
Abstract
OBJECTIVE: To study the effect of dengue virus infection on the production of endothelin 1(ET-1) and prostacyclin 2(PGI2) by human umbilical cord vein endothelial cells (HUVECs). METHODS: HUVECs were infected by dengue-2 virus (DV-2), the culture supernatants were collected at 4, 24, 48, 72 and 96 hours postinfection, and the levels of ET-1 and PGI2 were measured by radio-immunoassay. RESULTS: The results showed that inhibition of production of ET-1 and PGI2 was induced by dengue virus infection in HUVECs. Marked inhibition of ET-1 and PGI2 production was observed as early as 4 h postinfection and the inhibitory effect continued until 96 h postinfection. Significant differences were shown between the ET-1 concentration of the virus-infected and non-infected cells. Nevertheless, the inhibitory effect of dengue virus infection on the production of PGI2 gradually decreased and the PGI2 concentration reverted to normal level at 96 h postinfection. No significant difference between the PGI2 concentration of the virus-infected and non-infected cells was seem. CONCLUSION: The present study suggests that dengue virus infection of vascular endothelial cells could affect their normal functions of secretion of vasoactive substances, resulting in increased vascular permeability and impairment of homostasis and blood coagulation. Therefore, functional impairment of vascular endothelial cells induced by dengue virus might be an important aspect in the pathogenesis of DHF/DSS.
OBJECTIVE: To study the effect of dengue virus infection on the production of endothelin 1(ET-1) and prostacyclin 2(PGI2) by human umbilical cord vein endothelial cells (HUVECs). METHODS: HUVECs were infected by dengue-2 virus (DV-2), the culture supernatants were collected at 4, 24, 48, 72 and 96 hours postinfection, and the levels of ET-1 and PGI2 were measured by radio-immunoassay. RESULTS: The results showed that inhibition of production of ET-1 and PGI2 was induced by dengue virus infection in HUVECs. Marked inhibition of ET-1 and PGI2 production was observed as early as 4 h postinfection and the inhibitory effect continued until 96 h postinfection. Significant differences were shown between the ET-1 concentration of the virus-infected and non-infected cells. Nevertheless, the inhibitory effect of dengue virus infection on the production of PGI2 gradually decreased and the PGI2 concentration reverted to normal level at 96 h postinfection. No significant difference between the PGI2 concentration of the virus-infected and non-infected cells was seem. CONCLUSION: The present study suggests that dengue virus infection of vascular endothelial cells could affect their normal functions of secretion of vasoactive substances, resulting in increased vascular permeability and impairment of homostasis and blood coagulation. Therefore, functional impairment of vascular endothelial cells induced by dengue virus might be an important aspect in the pathogenesis of DHF/DSS.