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ABSTRACT: Flock House virus puff particle

PROVIDER: PRJNA1098227 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28602532.fastq.gz	Fastqsanger.gz
	SRR28602533.fastq.gz	Fastqsanger.gz
	SRR28602534.fastq.gz	Fastqsanger.gz
	SRR28602535.fastq.gz	Fastqsanger.gz
	SRR28602536.fastq.gz	Fastqsanger.gz

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Project description:Virus infections induce cellular gene up and down regulation, and these changes often provide clues to cellular pathways utilized by viruses. We used microarrays to examine the transcriptional responses of cultured Drosophila S2 cells to Flock House virus (FHV) replicon induction. Experiment Overall Design: Cultured S2 cells stably transfected with either a control replicon (pS2F1fs) or an FHV RNA1 replicon (pS2F1) were induced with 1 mM copper and we measured global transcript levels at 18 h after induction using Affymetrix Drosophila Genome 2.0 microarray chips.

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Lung emphysema can be elicited by nanoparticle triggered, p38 MAPK mediated virus reactivation

Project description:Environmental particle inhalation and persistent herpesvirus infection are omnipresent and associated with chronic lung diseases. Previously, we showed that pulmonary exposure to soot-like carbonaceous nanoparticles (CNP) or fibre-shaped engineered double-walled carbon nanotubes (DWCNT) induced an increase of lytic virus protein expression in latently murine gammaherpesvirus 68 (MHV-68) infected mouse lungs, with a similar pattern as acute infection suggesting virus reactivation. However, the molecular mechanisms underlying herpesvirus reactivation as well as herpesvirus reactivation associated disease exacerbation caused by particle exposure remain unclear. Here, we investigated the effects of environmental relevant repeated particle exposure and herpesvirus reactivation mechanistically, and therapeutically. In the MHV-68 mouse model, we identified elevated lung inflammation and emphysema-like injury after repetitive CNP exposure. We further uncovered that CNP reactivated latent herpesvirus mainly in CD11b+ macrophages. Mechanistically, ERK1/2, JNK and p38 MAPK were rapidly activated after CNP and DWCNT exposure in persistently MHV-68 infected bone marrow-derived macrophages, followed by upregulation of viral gene expression and increased viral titer but without generating a pro-inflammatory transcriptional signature. Pharmacological inhibition of p38 activation abrogated CNP but not DWCNT triggered virus reactivation. In vivo, p38 inhibitor pretreatment of latently infected mice also attenuated CNP exposure induced MHV-68 reactivation. Our findings suggest that particle pollution is an environmental challenge to trigger herpesvirus reactivation and related chronic lung disease by activating latent herpesvirus via p38 MAPK dependent signalling. Pharmacological p38 inhibition might serve as a protective target to alleviate particle exposure related chronic lung disease exacerbations.

2023-09-29 | GSE223818 | GEO

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