Virology
Volume 410, Issue 2, 20 February 2011, Pages 410?417
Antioxidant defense is one of the mechanisms by which mosquito cells survive dengue 2 viral infection
Tien-Huang Chena, 1,
Petrus Tanga, b, c, 1,
Chao-Fu Yanga,
Lin-Hsien Kaoa,
Yin-Ping Loa,
Ching-Kai Chuanga,
Yu-Tzu Shihb,
Wei-June Chena, b, ,
a Graduate Institute of Biomedical Sciences, Chang Gung University, Kwei-San, Tao-Yuan, 33332, Taiwan
b Department of Public Health and Parasitology, Chang Gung University, Kwei-San, Tao-Yuan, 33332, Taiwan
c Bioinformatics Center, Chang Gung University, Kwei-San, Tao-Yuan, 33332, Taiwan
Received 7 October 2010, Revised 24 November 2010, Accepted 9 December 2010, Available online 8 January 2011
DOI: 10.1016/j.virol.2010.12.013
Under an Elsevier user license
Abstract
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.
