Ultrastructural aspects of the replication of dengue virus type 2 isolated in Brazil

Barth, Ortrud Monika; Côrtes, Luzia M. C.; Filho, José Farias; Schatzmayr, Hermann G.

doi:10.1590/s0074-02761996000200025

Cited by 3 publications

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“…Electron microscopy analysis of ZIKV-infected primary skin fibroblasts showed the presence of membrane vesicles 70 to 100 nm in size that were located in intimate association with the ER, indicating that ZIKV replication occurs in close association with host cell membranes [ 29 ]. Such vesicular compartments were commonly observed in C6/36 cells infected with DENV [ 43 , 44 , 45 ]. YFV, WNV and DENV generate ER invaginations measuring 80–100 nm in diameter.…”

Section: Discussionmentioning

confidence: 99%

Structural investigation of C6/36 and Vero cell cultures infected with a Brazilian Zika virus

et al. 2017

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Zika virus (ZIKV) is a member of the flavivirus genus, and its genome is approximately 10.8 kilobases of positive-strand RNA enclosed in a capsid and surrounded by a membrane. Studies on the replication dynamics of ZIKV are scarce, which limits the development of antiviral agents and vaccines directed against ZIKV. In this study, Aedes albopictus mosquito lineage cells (C6/36 cells) and African green monkey kidney epithelial cells (Vero cells) were inoculated with a ZIKV sample isolated from a Brazilian patient, and the infection was characterized by immunofluorescence staining, phase contrast light microscopy, transmission electron microscopy and real-time RT-PCR. The infection was observed in both cell lineages, and ZIKV particles were observed inside lysosomes, the rough endoplasmic reticulum and viroplasm-like structures. The susceptibility of C6/36 and Vero cells to ZIKV infection was demonstrated. Moreover, this study showed that part of the replicative cycle may occur within viroplasm-like structures, which has not been previously demonstrated in other flaviviruses.

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Section: Discussionmentioning

confidence: 99%

Structural investigation of C6/36 and Vero cell cultures infected with a Brazilian Zika virus

et al. 2017

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“…The UPR was also identified in mosquito cells with DENV2 infection [ 8 ]. However, it usually does not impair the growth of those cells [ 13 ], frequently leading to persistent infection in mosquito cells [ 14 , 15 ]. Regulation of the UPR via virus-controlled translation of cellular proteins could be critical for a cell’s fate during infection in both mammalian and mosquito cells.…”

Section: Introductionmentioning

confidence: 99%

PERK Signal-Modulated Protein Translation Promotes the Survivability of Dengue 2 Virus-Infected Mosquito Cells and Extends Viral Replication

Hou

Chen

Chiang

et al. 2017

Viruses

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Survival of mosquitoes from dengue virus (DENV) infection is a prerequisite of viral transmission to the host. This study aimed to see how mosquito cells can survive the infection during prosperous replication of the virus. In C6/36 cells, global protein translation was shut down after infection by DENV type 2 (DENV2). However, it returned to a normal level when infected cells were treated with an inhibitor of the protein kinase RNA (PKR)-like ER kinase (PERK) signaling pathway. Based on a 7-Methylguanosine 5′-triphosphate (m7GTP) pull-down assay, the eukaryotic translation initiation factor 4F (eIF4F) complex was also identified in DENV2-infected cells. This suggests that most mosquito proteins are synthesized via canonical cap-dependent translation. When the PERK signal pathway was inhibited, both accumulation of reactive oxygen species and changes in the mitochondrial membrane potential increased. This suggested that ER stress response was alleviated through the PERK-mediated shutdown of global proteins in DENV2-infected C6/36 cells. In the meantime, the activities of caspases-9 and -3 and the apoptosis-related cell death rate increased in C6/36 cells with PERK inhibition. This reflected that the PERK-signaling pathway is involved in determining cell survival, presumably by reducing DENV2-induced ER stress. Looking at the PERK downstream target, α-subunit of eukaryotic initiation factor 2 (eIF2α), an increased phosphorylation status was only shown in infected C6/36 cells. This indicated that recruitment of ribosome binding to the mRNA 5′-cap structure could have been impaired in cap-dependent translation. It turned out that shutdown of cellular protein translation resulted in a pro-survival effect on mosquito cells in response to DENV2 infection. As synthesis of viral proteins was not affected by the PERK signal pathway, an alternate mode other than cap-dependent translation may be utilized. This finding provides insights into elucidating how the PERK signal pathway modulates dynamic translation of proteins and helps mosquito cells survive continuous replication of the DENV2. It was ecologically important for virus amplification in mosquitoes and transmission to humans.

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“…The following steps require centrifugation, usually at least at 1,500 rpm. This attack results in morphological distortions and cell deformation ( Barth 1992 , 2000 , 2010 , Barth et al 1996 ).…”

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confidence: 99%

Low impact to fixed cell processing aiming transmission electron microscopy

Barth

Silva

2016

Mem. Inst. Oswaldo Cruz

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Ultrastructural aspects of the replication of dengue virus type 2 isolated in Brazil

Cited by 3 publications

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Structural investigation of C6/36 and Vero cell cultures infected with a Brazilian Zika virus

Structural investigation of C6/36 and Vero cell cultures infected with a Brazilian Zika virus

PERK Signal-Modulated Protein Translation Promotes the Survivability of Dengue 2 Virus-Infected Mosquito Cells and Extends Viral Replication

Low impact to fixed cell processing aiming transmission electron microscopy

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