Dengue virus-2 infection hinders autophagosome–lysosome fusion and autophagy–lysosomal degradation pathway in human umbilical vein endothelial cells

Abstract

Autophagy plays a significant role in antiviral responses. Studies have shown that dengue virus-2 (DENV-2) activates autophagy, causing the endothelial cell injury. However, it remains unclear whether this injury is linked to the whole process of autophagy. This paper aimed to investigate the effects of DENV-2 on autophagic vesicle formation, autophagosome–lysosome fusion, and lysosomal degradation pathway in human umbilical vein endothelial cells (HUVECs). It is found that DENV-2 infection caused the formation of autophagic vesicles and increased the LC3 expression. The expression level of p62, STX17, SNAP29, and VAMP8 increased significantly in the late DENV-2 infection. Additionally, a high number of brighter lysosomal red fluorescent spots in the cytoplasm were observed after DENV-2 infection. In conclusion, DENV-2 infection activated autophagy and induced the formation of autophagic vesicles, but hindered the autophagosome–lysosome fusion and damaged the normal lysosomal acidification, thus blocking the autophagic flux.