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Latent human herpesvirus 6 is reactivated in chimeric antigen receptor T cells

ABSTRACT: Latent human herpesvirus 6 is reactivated in chimeric antigen receptor T cells

PROVIDER: PRJNA863599 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR20710641_1.fastq.gz	Fastqsanger.gz
	SRR20710641_2.fastq.gz	Fastqsanger.gz
	SRR20710642_1.fastq.gz	Fastqsanger.gz
	SRR20710642_2.fastq.gz	Fastqsanger.gz

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Latent human herpesvirus 6 is reactivated in chimeric antigen receptor T cells

Project description:Cell therapies have yielded durable clinical benefits for patients with cancer but have been accompanied by unexpected side effects of treatment, including neurotoxicity. Currently, we lack a comprehensive understanding of the mechanisms of toxicity observed in patients receiving cell therapies, including encephalitis caused by human herpesvirus 6 (HHV-6) that has been repeatedly reported. Here, via comprehensive viral RNA data mining, we examine the landscape of human latent viral reactivation, revealing that HHV-6B can become reactivated in human CD4+ T cells in standard in vitro cultures. Using single-cell sequencing, we identify a rare population of HHV-6 'super-expressors' (~1 in 360-10,000 cells) that possess high viral transcriptional activity in chimeric antigen receptor (CAR) T cell culture before spreading rapidly to infect other cells in vitro. Through the reanalysis of single-cell sequencing data from FDA-approved cell therapy products, we identify the presence of CAR+, HHV-6 super-expressor T cells in human patients in vivo. Together, our study implicates cell therapy products as the source of lytic HHV-6 repeatedly reported in clinical trialsand has broad implications for the design, screening, and interpretation of unexpected toxicities in cell therapies.

2023-08-05 | GSE210063 | GEO

Helminth Infection Reactivates Latent γ-herpesvirus Via Cytokine Competition at a Viral Promoter

Project description:Mammals are co-infected by multiple pathogens that interact through unknown mechanisms. We found that helminth infection, characterized by the induction of the cytokine interleukin-4 (IL-4) and the activation of the transcription factor Stat6, reactivated murine gammaherpesvirus infection in vivo. IL-4 promoted viral replication and blocked the antiviral effects of interferon-g (IFNg) by inducing Stat6 binding to the promoter for an important viral transcriptional transactivator. IL-4 also reactivated human Kaposi's sarcoma associated herpesvirus from latency in cultured cells. Exogenous IL-4 plus blockade of IFNg reactivated latent murine gammaherpesvirus infection in vivo, suggesting a âtwo-signalâ model for viral reactivation. Thus chronic herpesvirus infection, a component of the mammalian virome, is regulated by the counterpoised actions of multiple cytokines on viral promoters that have evolved to sense host immune status. All of the RNA from virus-pos cells and 50 ng of RNA from virus-neg cells was prepared for RNA-seq using ScriptSeq v2 RNA-seq library preparation kit (Epicentre). Index Primers (Epicentre) were added and samples underwent Duplex-Specific thermostable nuclease (DSN) (Evrogen) treatment to remove ribosomal RNA. Samples were pooled and sequenced on HiSeq.

2014-06-26 | E-GEOD-58116 | biostudies-arrayexpress

Helminth Infection Reactivates Latent γ-herpesvirus Via Cytokine Competition at a Viral Promoter

Project description:Mammals are co-infected by multiple pathogens that interact through unknown mechanisms. We found that helminth infection, characterized by the induction of the cytokine interleukin-4 (IL-4) and the activation of the transcription factor Stat6, reactivated murine gammaherpesvirus infection in vivo. IL-4 promoted viral replication and blocked the antiviral effects of interferon-g (IFNg) by inducing Stat6 binding to the promoter for an important viral transcriptional transactivator. IL-4 also reactivated human Kaposi's sarcoma associated herpesvirus from latency in cultured cells. Exogenous IL-4 plus blockade of IFNg reactivated latent murine gammaherpesvirus infection in vivo, suggesting a ‘two-signal’ model for viral reactivation. Thus chronic herpesvirus infection, a component of the mammalian virome, is regulated by the counterpoised actions of multiple cytokines on viral promoters that have evolved to sense host immune status.

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ZIC2 ChIP-Seq in KSHV latent and lytic reactivated BCBL-1 cells

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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).

2022-02-15 | GSE179864 | GEO

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