Antioxidant defense is one of the mechanisms by which mosquito cells survive dengue 2 viral infection

Chen, Tien-Huang; Tang, Petrus; Yang, Chia‐Ling; Kao, Lin-Hsien; Lo, Yu Lun; Chuang, Ching-Kai; Shih, Yuh-Chuan; Chen, Wei-June

doi:10.1016/j.virol.2010.12.013

Cited by 65 publications

(79 citation statements)

References 54 publications

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“…[31][32][33] It is therefore of relevance to determine if VEEV infection will impact insect cells and lead to accumulation of ROS in a similar manner as we observed in U87MG cells. We studied whether infection of mosquito cells with TC-83 would lead to a disruption of mitochondrial function.…”

Section: Veev Infection Results In Loss Of Mitochondrial Membrane Potmentioning

confidence: 73%

“…It has been demonstrated that in the case of flavivirus infections, infected insect cells show changes in antioxidant mechanisms that decrease the extent of cell death. [31][32][33] It has been demonstrated for Dengue virus that infected mosquito cells mounted a stronger antioxidant response by synthesising antioxidant enzymes (elevation of Glutathione S-transferase activity). 48 Mitochondrial distribution in cells and mitochondrial mobility are essential features of healthy cells.…”

Section: Discussionmentioning

confidence: 99%

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Altered mitochondrial dynamics as a consequence of Venezuelan Equine encephalitis virus infection

et al. 2017

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Mitochondria are sentinel organelles that are impacted by various forms of cellular stress, including viral infections. While signaling events associated with mitochondria, including those activated by pathogen associated molecular patterns (PAMPs), are widely studied, alterations in mitochondrial distribution and changes in mitochondrial dynamics are also beginning to be associated with cellular insult. Cells of neuronal origin have been demonstrated to display remarkable alterations in several instances, including neurodegenerative disorders. Venezuelan Equine Encephalitis Virus (VEEV) is a New World alphavirus that infects neuronal cells and contributes to an encephalitic phenotype. We demonstrate that upon infection by the vaccine strain of VEEV (TC-83), astrocytoma cells experience a robust drop in mitochondrial activity, which corresponds with an increased accumulation of reactive oxygen species (ROS) in an infection-dependent manner. Infection status also corresponds with a prominent perinuclear accumulation of mitochondria. Cellular enzymatic machinery, including PINK1 and Parkin, appears to be enriched in mitochondrial fractions as compared with uninfected cells, which is indicative of mitochondrial damage. Dynamin related protein 1 (Drp1), a protein that is associated with mitochondrial fission, demonstrated a modest enrichment in mitochondrial fractions of infected cells. Treatment with an inhibitor of mitochondrial fission, Mdivi-1, led to a decrease in caspase cleavage, suggesting that mitochondrial fission was likely to contribute to apoptosis of infected cells. Finally, our data demonstrate that mitophagy ensues in infected cells. In combination, our data suggest that VEEV infection results in significant changes in the mitochondrial landscape that may influence pathological outcomes in the infected cell.

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Section: Veev Infection Results In Loss Of Mitochondrial Membrane Potmentioning

confidence: 73%

Section: Discussionmentioning

confidence: 99%

Altered mitochondrial dynamics as a consequence of Venezuelan Equine encephalitis virus infection

et al. 2017

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“…Meanwhile, this enzyme also reduces O 2 to superoxide, leading to cellular oxidative stress [45]. Previous studies reported the generation of superoxide in mosquito cells during DENV infection [46], and the overexpression of quinone oxidoreductase has been recognized as the major contributor to reactive oxygen species formation [47]. Since the accumulation of this enzyme in the midgut of DENV-infected mosquito was observed [48], the biological interaction between DENV-2 prM protein and A. aegypti NADH-ubiquinone oxidoreductase may be the major contributor in the regulation of the oxido-reduction mechanism to manipulate DENV infection in mosquitoes.…”

Section: Discussionmentioning

confidence: 99%

Protein-protein interactions between A. aegypti midgut and dengue virus 2: two-hybrid screens using the midgut cDNA library

Tham

Balasubramaniam

Chew

et al. 2015

J Infect Dev Ctries

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Introduction: Dengue virus (DENV) is principally transmitted by the Aedes aegypti mosquito. To date, mosquito population control remains the key strategy for reducing the continuing spread of DENV. The focus on the development of new vector control strategies through an understanding of the mosquito-virus relationship is essential, especially targeting the midgut, which is the first mosquito organ exposed to DENV infection. Methodology: A cDNA library derived from female adult A. aegypti mosquito midgut cells was established using the switching mechanism at the 5' end of the RNA transcript (SMART), in combination with a highly potent recombination machinery of Saccharomyces cerevisiae. Gal4-based yeast two-hybrid (Y2H) assays were performed against DENV-2 proteins (E, prM, M, and NS1). Mammalian two-hybrid (M2H) and double immunofluorescence assays (IFA) were conducted to validate the authenticity of the three selected interactions.Results: The cDNA library was of good quality based on its transformation efficiency, cell density, titer, and the percentage of insert size. A total of 36 midgut proteins interacting with DENV-2 proteins were identified, some involved in nucleic acid transcription, oxidoreductase activity, peptidase activity, and ion binding. Positive outcomes were obtained from the three selected interactions validated using M2H and double IFA assays. Conclusions: The identified proteins have different biological activities that may aid in the virus replication pathway. Therefore, the midgut cDNA library is a valuable tool for identifying DENV-2 interacting proteins. The positive outcomes of the three selected proteins validated supported the quality of the cDNA library and the robustness of the Y2H mechanisms.

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“…Dengue virus-infected mosquito cells continued growing, implying that an anti-ER stress factor might be involved in the process of viral replication in mosquito cells [25]. Mosquito cells trigger a pathway that protects infected cells from death, which might be how Aedes mosquitoes resist dengue virus infection [26]. Activation of the UPR to cope with ER stress in the early phase of viral infection was shown in various vertebrate cells [27,28].…”

Section: Discussionmentioning

confidence: 99%

Chikungunya Virus Induces a More Moderate Cytopathic Effect in Mosquito Cells than in Mammalian Cells

Siripanyaphinyo²,

Tumkosit³

et al. 2012

Intervirology

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Objectives: Chikungunya virus (CHIKV) is an alphavirus belonging to the Togaviridae family. Alphaviruses cause a chronic non-cytopathic infection in mosquito cells, while they develop a highly cytopathic infection in cells originating from various vertebrates. In this study, we compared the cytopathic effect (CPE) induced by CHIKV in Vero cells and a mosquito cell line, C6/36 cells. Methods: CPE and the virus titers were compared between the CHIKV-infected C6/36 and Vero cells. Apoptosis was measured by TUNEL assay, and the differences between the C6/36 and Vero cells were compared. Results: CHIKV infection induced strong CPE and apoptosis in the Vero cells, but light CPE in the C6/36 cells. The virus titers produced in the C6/36 cells were much higher than those produced in the Vero cells. Conclusions: The reason CHIKV induced strong CPE is that this virus triggers strong apoptosis in Vero cells compared with C6/36 cells. CHIKV established a persistent infection in C6/36 cells after being passaged 20 times. CHIKV infection in mosquito cells was distinct from that in Vero cells. The cell and species specificity of CHIKV-induced cell death implies that the cellular and viral regulators involved in apoptosis may play an important role in determining the outcome of CHIKV infection.

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Antioxidant defense is one of the mechanisms by which mosquito cells survive dengue 2 viral infection

Cited by 65 publications

References 54 publications

Altered mitochondrial dynamics as a consequence of Venezuelan Equine encephalitis virus infection

Altered mitochondrial dynamics as a consequence of Venezuelan Equine encephalitis virus infection

Protein-protein interactions between A. aegypti midgut and dengue virus 2: two-hybrid screens using the midgut cDNA library

Chikungunya Virus Induces a More Moderate Cytopathic Effect in Mosquito Cells than in Mammalian Cells

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