Abstract
Cytopathic effects (CPEs) in mosquito cells are generally trivial compared to those that occur in mammalian cells, which usually end up undergoing apoptosis during dengue virus (DENV) infection. However, oxidative stress was detected in both types of infected cells. Despite this, the survival of mosquito cells benefits from the upregulation of genes related to antioxidant defense, such as glutathione S transferase (GST). A second defense system, i.e., consisting of antiapoptotic effects, was also shown to play a role in protecting mosquito cells against DENV infection. This system is regulated by an inhibitor of apoptosis (IAP) that is an upstream regulator of caspases-9 and -3. DENV-infected C6/36 cells with double knockdown of GST and the IAP showed a synergistic effect on activation of these two caspases, causing a higher rate of apoptosis (>20%) than those with knockdown of each single gene (∼10%). It seems that the IAP acts as a second line of defense with an additional effect on the survival of mosquito cells with DENV infection. Compared to mammalian cells, residual hydrogen peroxide in DENV-infected C6/36 cells may signal for upregulation of the IAP. This novel finding sheds light on virus/cell interactions and their coevolution that may elucidate how mosquitoes can be a vector of DENV and probably most other arboviruses in nature.
Highlights
The dengue virus (DENV), a flavivirus belonging to the family Flaviviridae, is the etiological agent of dengue fever (DF), dengue hemorrhagic fever (DHF), and dengue shock syndrome (DSS) [1]
This study demonstrated an idea that mosquito cells can survive dengue virus infection through antioxidant defense and an additional effect by induction of inhibitor of apoptosis (IAP) expression for protection of infection
We preliminarily identified an inhibitor of apoptosis (IAP) gene that is upregulated in mosquito cells with DENV infection
Summary
The dengue virus (DENV), a flavivirus belonging to the family Flaviviridae, is the etiological agent of dengue fever (DF), dengue hemorrhagic fever (DHF), and dengue shock syndrome (DSS) [1]. The DENV and other viruses generally invade a host cell by redirecting cellular processes in order to meet the needs of viral propagation. During infection by the DENV, an unfolded protein response (UPR), or so-called UPR signal cascade, is usually induced in a time-dependent manner [7]; it may be able to cope with endoplasmic reticular (ER) stress in host cells [8]. The UPR can provide an early defensive mechanism for infected cells to survive ER stress due to viral infection by eliminating misfolded proteins and allowing cells to recover. The cell type may play a role in determining responses to viral infections, leading to differential fates of infected cells [12]
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