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A herpesvirus microRNA targets host microRNA processing to promote virus reactivation from latency [Latent reactivation]

ABSTRACT: A herpesvirus microRNA targets host microRNA processing to promote virus reactivation from latency [Latent reactivation]

PROVIDER: PRJNA745356 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15096382.fastq.gz	Fastqsanger.gz
	SRR15096383.fastq.gz	Fastqsanger.gz
	SRR15096384.fastq.gz	Fastqsanger.gz
	SRR15096385.fastq.gz	Fastqsanger.gz
	SRR15096386.fastq.gz	Fastqsanger.gz

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A herpesvirus microRNA targets host microRNA processing to promote virus reactivation from latency [Latent reactivation]

Project description:In a major study, we found that miR-aU14, a potential miRNA expressed by human herpesvirus 6A (HHV-6A), acts to selectively inhibit the processing of members of the human miR-30 family through direct RNA:RNA interaction and causes changes in mitochondrial arcchitecture through p53-Drp1 axis. In order to characterize miR-aU14 during virus reactivation, we carried out small RNA-seq from U2-OS cells carrying latent HHV-6A. Virus reactivation was carried out using 80 ng/ml of Trichostatin-A (TSA).

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A herpesvirus microRNA targets host microRNA processing to promote virus reactivation from latency

Project description:A herpesvirus microRNA targets host microRNA processing to promote virus reactivation from latency

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A herpesvirus microRNA targets host microRNA processing to promote virus reactivation from latency [Lytic infection]

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Project description:HHV-6A is a human herpesvirus that integrates into human sub telomeric regions to acquire latency. This latent virus frequently reactivates causing numerous diseases. The project was aimed to understand changes in host cell prteomics upon virus reactivation, which might helpin understanding the pathophysiology of virus reactivation.

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A herpesvirus microRNA targets host microRNA processing to promote virus reactivation from latency [Lytic infection]

Project description:A herpesvirus microRNA targets host microRNA processing to promote virus reactivation from latency [Lytic infection]

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Project description:A herpesvirus microRNA targets host microRNA processing to promote virus reactivation from latency [dRNA-seq]

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Stress triggers expression of bovine herpesvirus 1 infected cell protein 4 (bICP4) RNA during early stages of reactivation from latency in pharyngeal tonsil

Project description:Bovine herpesvirus 1 (BoHV-1), an important pathogen of cattle, establishes lifelong latency in sensory neurons within trigeminal ganglia (TG) after acute infection. The BoHV-1 latency-reactivation cycle, like other -herpesvirinae subfamily members, is essential for viral persistence and transmission. Notably, cells within pharyngeal tonsil (PT) also support a quiescent or latent BoHV-1 infection. The synthetic corticosteroid dexamethasone, which mimics the effects of stress, consistently induces BoHV-1 reactivation from latency allowing early stages of viral reactivation to be examined in the natural host. Based on previous studies, we hypothesized that stress-induced cellular factors trigger expression of key viral transcriptional regulatory genes. To explore this hypothesis, RNA-sequencing studies compared viral gene expression in PT during early stages of dexamethasone-induced reactivation from latency. Strikingly, RNA encoding infected cell protein 4 (bICP4), which is translated into an essential viral transcriptional regulatory protein, was detected 30 minutes after dexamethasone treatment. Ninety minutes after dexamethasone treatment bICP4 and to a lesser extent bICP0 RNA were detected in PT. All lytic cycle viral transcripts were detected within three hours after dexamethasone treatment. Surprisingly, the latency related (LR) gene, the only viral gene abundantly expressed in latently infected TG neurons, was not detected in PT during latency. In TG neurons, bICP0 and the viral tegument protein VP16 are expressed before bICP4 during reactivation suggesting distinct viral regulatory genes mediate reactivation from latency in PT versus TG neurons. Finally, these studies confirm PT is a biologically relevant site for BoHV-1 latency, reactivation from latency, and virus transmission.

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Project description:Epstein-Barr virus (EBV) uses a biphasic lifecycle of latency and lytic reactivation to infect >95% of adults worldwide. Despite its central role in EBV persistence and oncogenesis, much remains unknown about how EBV latency is maintained. We used a human genome-wide CRISPR/Cas9 screen to identify that the nuclear protein SFPQ was critical for latency. SFPQ supported expression of linker histone H1, which stabilizes nucleosomes and regulates nuclear architecture, but has not been previously implicated in EBV gene regulation. H1 occupied latent EBV genomes, including the immediate early gene BZLF1 promoter. Upon reactivation, SFPQ was sequestered into sub-nuclear puncta, and EBV genomic H1 occupancy diminished. Enforced H1 expression blocked EBV reactivation upon SFPQ knockout, confirming it as necessary downstream of SFPQ. SFPQ knockout triggered reactivation of EBV in B and epithelial cells as well as in Kaposi’s Sarcoma Associated Herpesvirus, suggesting a conserved gamma-herpesvirus role. These findings highlight SFPQ as a major regulator of H1 expression and EBV latency.

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