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Nuclear Lamina binds the EBV genome during latency and regulates viral gene expression

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens human gammaherpesvirus 4

PROVIDER: GSE198413 | GEO | 2022/03/11

REPOSITORIES: GEO

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The Nuclear Lamina Binds the EBV Genome During Latency and Regulates Viral Gene Expression

Project description:Several cellular factors, including the nuclear lamina, regulate chromatin composition and architecture. While the interaction of the viral genome with the nuclear lamina has been studied in the context of EBV lytic reactivation, the role of the nuclear lamina in controlling EBV latency has not been investigated. Here, we report that the nuclear lamina is an essential epigenetic regulator of the EBV episome.

2022-03-18 | GSE198954 | GEO

Nuclear lamina binds the EBV genome during latency and regulates viral gene expression [Hi-C]

Project description:Approximately 90% of the world population is infected with EBV and carries the virus in a silent, asymptomatic state for life. In immunocompromised individuals, EBV infection can cause B-cell transformation and malignancies. One approach to control EBV infectivity is by changing the expression of viral genes. We are interested in how epigenetics contributes to regulating the gene expression patterns adopted by EBV during latency. The host’s hijacking is a well know strategy adopted by viruses to modify the epigenome, the transcriptome and the proteome of the host with the aim to survive and remain silent in the host. We observed that in B cells, EBV infection mimics antigen-mediated activation, resulting in the induction of specific proteins named Lamin A/C. Lamins have multiple and central roles: they provide nuclear physical support, anchor the heterochromatin to the nuclear periphery and seem to play a role in several nuclear functions requiring the chromatin structure rearrangement. The interaction with lamins has already been studied in the context of EBV lytic reactivation, but their role in the control of the EBV latency states and as epigenetic regulators of different EBV genes expression profiles has not been investigated. The binding of the Lamin AC to important regulatory regions of EBV genome was assessed through ChIP-Seq, and gene expression (RNA-Seq) profiles were evaluated in wild type and Lamin AC KO cell lines. Differences in protein and RNA expressions in B cells activated by using both EBV and a simulation of the immune response were analyzed. Our data suggest two main conclusions: lamins might contribute to the epigenetic control of EBV genes expression during latency changing the interaction of the host structural proteins with key regulatory regions in the viral genome and a possible mechanism with who EBV modifies the nucleus and hijacks cellular mechanisms.

2022-04-08 | GSE198412 | GEO

Nuclear Lamina binds the EBV genome during latency and regulates viral gene expression [RNA-seq]

Project description:Approximately 90% of the world population is infected with EBV and carries the virus in a silent, asymptomatic state for life. In immunocompromised individuals, EBV infection can cause B-cell transformation and malignancies. One approach to control EBV infectivity is by changing the expression of viral genes. We are interested in how epigenetics contributes to regulating the gene expression patterns adopted by EBV during latency. The host’s hijacking is a well know strategy adopted by viruses to modify the epigenome, the trascriptome and the proteome of the host with the aim to survive and remain silent in the host. We observed that in B cells, EBV infection mimics antigen-mediated activation, resulting in the induction of specific proteins named Lamin A/C. Lamins have multiple and central roles they: provide nuclear physical support; anchor the heterochromatin to the nuclear periphery and seem to play a role in several nuclear functions requing the chromatin structure rearrangement. The interaction with lamins has already been study in the context of EBV lytic reactivation, but their role in the control of the EBV latency states and as epigenetic regulators of different EBV genes expression profiles as not been investigated. The binding of the Lamin AC to important regulatory regions of EBV genome was assessed through ChIP-Seq and, and gene expression (RNA-Seq) profiles, were evaluated in wild type and Lamin AC KO cell lines. Differences in protein and RNA expressions in B cells activated by using both EBV and a simulation of the immune response were analyzed. Our data suggest two main conclusion: lamins might contribute to the epigenetic control of EBV genes expression during latency changing the interaction of the host structural proteins with key regulatory regions in the viral genome and a possible mechanism with who EBV modifies the nucleus and hijacks cellular mechanisms.

2022-03-11 | GSE181012 | GEO

Nuclear Lamina binds the EBV genome during latency and regulates viral gene expression

Project description:Nuclear Lamina binds the EBV genome during latency and regulates viral gene expression

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The Nuclear Lamina Binds the EBV Genome During Latency and Regulates Viral Gene Expression

Project description:The Nuclear Lamina Binds the EBV Genome During Latency and Regulates Viral Gene Expression

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Nuclear Lamina binds the EBV genome during latency and regulates viral gene expression [RNA-seq]

Project description:Nuclear Lamina binds the EBV genome during latency and regulates viral gene expression [RNA-seq]

| PRJNA750410 | ENA

Nuclear lamina binds the EBV genome during latency and regulates viral gene expression [Hi-C]

Project description:Nuclear lamina binds the EBV genome during latency and regulates viral gene expression [Hi-C]