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Replication of Dengue virus in differentiating K562-megakaryocytes is promoted by virus induced suppression in the accumulation of reactive oxygen species

ABSTRACT: Replication of Dengue virus in differentiating K562-megakaryocytes is promoted by virus induced suppression in the accumulation of reactive oxygen species

PROVIDER: PRJNA772576 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16477768_1.fastq.gz	Fastqsanger.gz
	SRR16477768_2.fastq.gz	Fastqsanger.gz
	SRR16477769_1.fastq.gz	Fastqsanger.gz
	SRR16477769_2.fastq.gz	Fastqsanger.gz
	SRR16477770_1.fastq.gz	Fastqsanger.gz

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Replication of Dengue virus in differentiating K562-megakaryocytes is promoted by virus induced suppression in the accumulation of reactive oxygen species

Project description:Our study reports that over-expression of NRf2 target genes causes reduction in the ROS accumulation in differentiating cells which ultimately enhances Dengue virus replication and we also report the suppression of cell adhesion molecules and platelet specific surface markers in Dengue virus infected K562-megakaryocyte cells.

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Replication of Dengue Virus in K562-Megakaryocytes Induces Suppression in the Accumulation of Reactive Oxygen Species.

Project description:Dengue virus can infect human megakaryocytes leading to decreased platelet biogenesis. In this article, we report a study of Dengue replication in human K562 cells undergoing PMA-induced differentiation into megakaryocytes. PMA-induced differentiation in these cells recapitulates steps of megakaryopoiesis including gene activation, expression of CD41/61 and CD61 platelet surface markers and accumulation of intracellular reactive oxygen species (ROS). Our results show differentiating megakaryocyte cells to support higher viral replication without any apparent increase in virus entry. Further, Dengue replication suppresses the accumulation of ROS in differentiating cells, probably by only augmenting the activity of the transcription factor NFE2L2 without influencing the expression of the coding gene. Interestingly pharmacological modulation of NFE2L2 activity showed a simultaneous but opposite effect on intracellular ROS and virus replication suggesting the former to have an inhibitory effect on the later. Also cells that differentiated while supporting intracellular virus replication showed reduced level of surface markers compared to uninfected differentiated cells.

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