Human betaherpesvirus 5
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA389726 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5660010_1.fastq.gz | Fastqsanger.gz | |||
| SRR5660010_2.fastq.gz | Fastqsanger.gz | |||
| SRR5660020_1.fastq.gz | Fastqsanger.gz | |||
| SRR5660020_2.fastq.gz | Fastqsanger.gz | |||
| SRR5660030_1.fastq.gz | Fastqsanger.gz |
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Project description:Abstract: The transcriptional program associated with herpesvirus latency and the viral genes regulating entry into and exit from latency are poorly understood and controversial. Here, we developed and validated a targeted enrichment platform and conducted large-scale transcriptome analyses of human cytomegalovirus (HCMV) infection. We used both an experimental hematopoietic cell model of latency, and cells from naturally infected, healthy human subjects (clinical) to define the breadth of viral genes expressed. The viral transcriptome derived from experimental infection was highly correlated with that from clinical infection, validating our experimental latency model. These transcriptomes revealed a broader profile of gene expression during infection in hematopoietic cells than previously appreciated. Further, using recombinant viruses that establish a non-reactivating, latent-like or replicative infection in CD34+ hematopoietic progenitors (HPCs), we defined classes of low to moderately expressed genes that are differentially regulated in latent vs. replicative states of infection. Most of these genes have yet to be studied in depth. By contrast, genes that were highly expressed, were expressed similarly in both latent and replicative infection. From these findings, a model emerges whereby low or moderately expressed genes may have the greatest impact on regulating the switch between viral latency and replication. The core set of viral genes expressed in natural infection and differentially regulated depending on the pattern of infection provides novel insight into the HCMV transcriptome associated with latency in the host and a resource for investigating new virus-host interactions underlying persistence. Significance: Herpesviruses have an extraordinarily complex relationship with their host, persisting for the lifetime of the host by way of a latent infection. Reactivation of replication is associated with significant disease risk, particularly in immunocompromised individuals. We characterize in depth transcriptional profiles of HCMV latency. We show that a broad and concordant viral transcriptome is found in both an experimental model of latency and in asymptomatically infected individuals. We further define genes that are differentially regulated during latent and replicative states- candidates for key regulators controlling the switch between latency and reactivation. This work will help understand the persistence of complex DNA viruses and provides a path towards developing antiviral strategies to control herpesvirus entry into and exit from latency.
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Project description:Primary infection with human cytomegalovirus (HCMV) results in a lifelong infection due to its ability to establish latent infection, with one characterized viral reservoir being hematopoietic cells. Although reactivation from latency causes serious disease in immunocompromised individuals, our molecular understanding of latency is limited. Here, we delineate viral gene expression during natural HCMV persistent infection by analyzing the massive transcriptome sequencing (RNA-seq) atlas generated by the Genotype-Tissue Expression (GTEx) project. This systematic analysis reveals that HCMV persistence in vivo is prevalent in diverse tissues. Notably, we find only viral transcripts that resemble gene expression during various stages of lytic infection with no evidence of any highly restricted latency-associated viral gene expression program. To further define the transcriptional landscape during HCMV latent infection, we also used single-cell RNA-seq and a tractable experimental latency model. In contrast to some current views on latency, we also find no evidence for any highly restricted latency-associated viral gene expression program. Instead, we reveal that latency-associated gene expression largely mirrors a late lytic viral program, albeit at much lower levels of expression. Overall, our work has the potential to revolutionize our understanding of HCMV persistence and suggests that latency is governed mainly by quantitative changes, with a limited number of qualitative changes, in viral gene expression.
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