Abstract: OBJECTIVE To explore the functional injuries of intestinal epithelial barrier（IEB） induced by dengue virus（DV） infection, so as to provide basic evidence for elucidating the mechanism of dengue hemorrhagic fever（DHF） and dengue shock syndrome（DSS）.METHODS Stable expression cell lines of RhoA mutant were infected with Dengue virus 2（DV2）, and the infectious effect were determined by viurs plaque assay. Based on the HMEC-CaCO₂ co-culture system, the IEB functional injuries resulted from DV infection and distribution and network structure of tight junction protein were observed. With DV infection, the secretion of IL-6 and IL-8 by vascular epithelial cells, synergized with lipopolysaccharide（LPS） stimulation, were determined by enzyme-linked immunosorbent assay（ELISA） and polymerase chain reaction（PCR）.RESULTS Interference of RhoA/ROCK pathway activity significantly restrained the proliferation of DENV2. Compared with the ECV304^N control, the titers of intracellular and supernatant of ECV^WtRhoA, ECV^{V14 RhoA} and ECV^{N19 RhoA} groups were significantly reduced by 88.40%, 51.17%, 25.33% or 35.83%, 15.21%, 10.63% respectively. Co-cultureed DV-infected HMEC with CaCO₂, transepithelial resistance（TER） was reduced by（27.00±4.55）Ω/cm² and（40.33±0.12）Ω/cm², respectively, compared to mock infection group at 24 h or 48 h postinfection（p.i）, accompanied with distribution alternation of tight junction protein ZO-1 and Occludin, damage of tightly connected webwork, and increased permeability of intestinal epithelial. In addition, under DV infection, compared with single infection group, synergized stimulation of LPS may further promote IL-8 and IL-6 secretion of vascular epithelial cells（P＜0.001）.CONCLUSION The dysfuction of intestinal epithelial barrier and bactrial translocation might be induced by cooperated participating of RhoA/ROCK pathway and other factors of DV-infected vascular epithelial cells, thereby initiating continuous stimulation on the vascular epithilial cells by LPS, which might be the accelerator of vascular epithelial injury and plasam leakage and drive the progress of DHS/DSS. However, the underlying mechanism need to be identified.