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HCMV epigenome and transcriptome during early lytic infection

ABSTRACT: HCMV epigenome and transcriptome during early lytic infection

PROVIDER: PRJNA719833 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14146035.fastq.gz	Fastqsanger.gz
	SRR14146035_1.fastq.gz	Fastqsanger.gz
	SRR14146035_2.fastq.gz	Fastqsanger.gz
	SRR14146036.fastq.gz	Fastqsanger.gz
	SRR14146036_1.fastq.gz	Fastqsanger.gz

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Project description:This SuperSeries is composed of the SubSeries listed below.

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Project description:Infection with Human cytomegalovirus (HCMV) can result in either productive or non-productive infection, the latter potentially leading to establishment of latency, but the molecular factors that dictate these different infection outcomes are elusive. Macrophages are known targets of HCMV and considered to be permissive for productive infection, while monocytes, their precursors, are thought to support latent infection. Here we reveal that infection of macrophages is more complex than previously appreciated and can result in either productive or non-productive infection. By analyzing the progression of HCMV infection in c and macrophages using single cell transcriptomics, we uncover that the key characteristics that define productive and non-productive cells are the onset of viral gene expression, and activation of Interferon-stimulated genes (ISGs), respectively. We show that the level of viral gene expression, and specifically the expression of the major immediate early factor, IE1, is the principle barrier for establishing productive infection. On the cellular side, induction of ISGs in response to infection surprisingly does not dictate infection outcome, but we find that the cell intrinsic ISG levels is a main determinant of infection outcome. Indeed, intrinsic ISG level is downregulated with monocyte differentiation. We further show that, compared to monocytes, non-productive macrophages maintain slightly higher levels of viral transcripts and are able to reactivate, raising the possibility that they can serve as latency reservoirs in tissues. Moreover, we find that productive infection perturbs macrophage identity and function, likely affecting their immunological role during active infection. Overall, by harnessing the tractable system of monocyte differentiation we decipher the underlying principles that control HCMV infection outcome, and propose macrophages as a new potential HCMV reservoir in tissues.

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