Abstract
Dengue fever is a mosquito-borne viral disease of increasing global importance. The disease has caused heavy burdens due to frequent outbreaks in tropical and subtropical areas of the world. The dengue virus (DENV) is generally transmitted between human hosts via the bite of a mosquito vector, primarily Aedes aegypti and Ae. albopictus as a minor species. It is known that the virus needs to alternately infect mosquito and human cells. DENV-induced cell death is relevant to the pathogenesis in humans as infected cells undergo apoptosis. In contrast, mosquito cells mostly survive the infection; this allows infected mosquitoes to remain healthy enough to serve as an efficient vector in nature. Overexpression of antioxidant genes such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione S-transferase (GST), glutaredoxin (Grx), thioredoxin (Trx), and protein disulfide isomerase (PDI) have been detected in DENV2-infected mosquito cells. Additional antioxidants, including GST, eukaryotic translation initiation factor 5A (eIF5a), and p53 isoform 2 (p53-2), and perhaps some others, are also involved in creating an intracellular environment suitable for cell replication and viral infection. Antiapoptotic effects involving inhibitor of apoptosis (IAP) upregulation and subsequent elevation of caspase-9 and caspase-3 activities also play crucial roles in the ability of mosquito cells to survive DENV infection. This article focused on the effects of intracellular responses in mosquito cells to infection primarily by DENVs. It may provide more information to better understand virus/cell interactions that can possibly elucidate the evolutionary pathway that led to the mosquito becoming a vector.
Highlights
Dengue viruses (DENVs) are members of the genus Flavivirus belonging to the familyFlaviviridae [1]; these viruses are naturally transmitted between humans via the bite of a mosquito vector
superoxide dismutase (SOD), CAT, and glutathione peroxidase (GPX) are defined as the first line of the defense grid that copes with oxidative stress induced in mosquito cells infected with DENV
Other relevant molecules, including glutathione S-transferase (GST), eIF5A, and p53-2, identified in DENV2-infected mosquito cells are involved in stress reduction and protection of infected cells
Summary
Flaviviridae [1]; these viruses are naturally transmitted between humans via the bite of a mosquito vector. Prevention of dengue transmission in most endemic or epidemic areas depends on the effective control of mosquito vectors [13]. In most areas with dengue outbreaks in the world, Aedes aegypti and/or Ae. albopictus are reported to be principal vectors, because both species are susceptible to viral infection and frequently choose humans as targets for a blood meal [18,19]. Prolonged survivability of the mosquito vector is obviously essential to produce large amounts of progeny virions [20]. DENV infection may offer an avenue to explore how the mosquito originally became a disease vector. DENV infection, which is required for sustainability of the natural cycle of viral replication and transmission
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