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ATRX reduces the accessibility of HCMV genomes during lytic infections

ABSTRACT: ATRX reduces the accessibility of HCMV genomes during lytic infections

PROVIDER: PRJNA1093462 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28504083_1.fastq.gz	Fastqsanger.gz
	SRR28504083_2.fastq.gz	Fastqsanger.gz
	SRR28504084_1.fastq.gz	Fastqsanger.gz
	SRR28504084_2.fastq.gz	Fastqsanger.gz
	SRR28504085.fastq.gz	Fastqsanger.gz

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ATRX reduces the accessibility of HCMV genomes during lytic infections

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Project description:Primary infection with Human cytomegalovirus (HCMV) results in a persistent lifelong infection due to its ability to establish latent infection. During productive HCMV infection, viral genes are expressed in a coordinated cascade that is characteristic of all herpesviruses and traditionally relies on the dependencies of viral genes on protein synthesis and viral DNA replication. In contrast, the transcriptional landscape associated with HCMV latency is still disputed and poorly understood. Here, we examine viral transcriptomic dynamics during the establishment of both productive and latent HCMV infections. These temporal measurements reveal that viral gene expression dynamics along productive infection and their dependencies on protein synthesis and viral DNA replication, do not fully align. This illustrates that the regulation of herpesvirus genes does not represent a simple sequential transcriptional cascade and surprisingly many viral genes are regulated by multiple independent modules. Using our improved classification of viral gene expression kinetics in conjunction with transcriptome-wide measurements of the effects of a wide array of chromatin modifiers, we unbiasedly show that a defining characteristic of latent cells is the unique repression of immediate early (IE) genes. In particular, we demonstrate that IE1 (a central IE protein) expression is the principal barrier for achieving a full productive cycle. Altogether, our findings provide an unbiased and elaborate definition of HCMV gene expression in lytic and latent infection states.

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N6-methyladenosine modification of HCMV IE1 transcript promotes the repressive state of viral genome to achieve latent infection

Project description:Human cytomegalovirus (HCMV) is a prevalent pathogen that chronically infects the majority of human population. Among the many features that allow such widespread HCMV infection, one is its ability to maintain a transcriptionally dormant immune-evasive state called latency by suppressing its own major immediate early promoter (MIEP) via epigenetic alterations. In this study, we show a novel mechanism of MIEP regulation in which the major immediate early (MIE) gene product, IE1, downregulates its own promoter activity in an m6A modification-dependent manner. We found that the loss of the m6A writer, METTL3, in host cell results in the failure of HCMV to establish latency in these cells. Through transcriptome-wide m6A profiling of latently infected monocytes, we identified that the major immediate early gene product IE1 is m6A-modified during latent infection, with an m6A profile that is distinct from that found during lytic infection. Using an IE1-specific m6A-abolished mutant, we found that latent infection-specific m6A modification of the IE1 transcript was necessary for the efficient repression of MIEP, and this mutant virus failed to establish latency and progressed toward lytic-like infection in THP-1 cells. Our findings demonstrate that HCMV exploits the host m6A machinery to suppress its own lytic program to establish latency and uncover an unexpected role of immediate early gene mRNA in regulating its own expression.

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