کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
3424704 | 1594265 | 2011 | 8 صفحه PDF | دانلود رایگان |

Dengue viruses (DENVs) generally induce apoptosis in mammalian cells but cause only minor damage in mosquito cells. To find genes involved in determining the cell fate, datasets derived from expressed sequence tags (ESTs) of C6/36 cells with and without infection were established. Of overexpressed genes found in infected dataset, chaperone proteins were validated significantly upregulated in C6/36 cells at 24 hpi. It suggests that DENV-2 in mosquito cells activates the unfolded protein response to cope with endoplasmic reticular stress. Changes in the mitochondrial membrane potential and generation of superoxide provided further evidence that DENV-2 induces oxidative stress in both C6/36 and BHK-21 cells. Significant elevation of glutathione S-transferase (GST) activity was shown in infected C6/36, but not BHK-21, cells, while suppression of GST produced superoxide at 36 hpi and increased the cell death rate at 48 hpi. This indicates that mosquito cells protect themselves against viral infection through antioxidant defenses.Research Highlights
► Elucidation on the response to DENV infection between mosquito and mammalian cells.
► Identification of ER-associated chaperones based on EST libraries of mosquito cells.
► Mosquito cells rescue themselves from DENV infection through antioxidant defenses.
► The first evidence of oxidative stress in mosquito cells against of DENV infection.
Journal: Virology - Volume 410, Issue 2, 20 February 2011, Pages 410–417