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Virus-like vesicles of Kaposi’s Sarcoma-Associated Herpesvirus activate lytic replication through triggering differentiation signaling

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

OTHER RELATED OMICS DATASETS IN: PRJNA356918PRJNA356917PRJNA356883

ORGANISM(S): Human gammaherpesvirus 8 Homo sapiens

PROVIDER: GSE91386 | GEO | 2017/05/03

SECONDARY ACCESSION(S): PRJNA356883

REPOSITORIES: GEO

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Virus-like vesicles of Kaposi’s Sarcoma-Associated Herpesvirus activate lytic replication through triggering differentiation signaling (microRNA)

Project description:Virus-like vesicles (VLVs) are membrane derived cellular vesicles that resemble native envelope viruses in organization and conformation, but lack viral capsid and/or genome. During productive virus infection, both infectious virions and non-infectious VLVs are produced and released into the extracellular space. VLVs have been shown to play a role in intercellular communication and in facilitating virus infection. The study of VLVs in the context of gammaherpesvirus infection has been largely restricted due to the technical difficulty of separating VLVs and virions. Here we report a strategy for using a KSHV mutant deficient in capsid assembly to isolate VLVs during infection. Using Mass Spectrometry analysis, we identified that VLVs contain viral glycoproteins required for cellular entry, and tegument proteins involved in regulating lytic replication. Functional analysis showed that VLVs could activate the RTA promoter, the lytic switch for KSHV, and further induce KSHV lytic gene expression from latency. We used RNA sequencing to do a genome-wide analysis of cellular responses triggered by VLVs, and revealed that PRDM1, a master regulator in cell differentiation, was up-regulated. Our data shows that VLVs play an important role in promoting KSHV lytic replication by inducing PRDM1 expression which activates the RTA promoter. Our study significantly extends our current understanding of VLVs.

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Virus-like vesicles of Kaposi’s Sarcoma-Associated Herpesvirus activate lytic replication through triggering differentiation signaling (mRNA)

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Virus-Like Vesicles of Kaposi's Sarcoma-Associated Herpesvirus Activate Lytic Replication by Triggering Differentiation Signaling.

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Virus-like vesicles of Kaposi’s Sarcoma-Associated Herpesvirus activate lytic replication through triggering differentiation signaling

Project description:Virus-like vesicles of Kaposi’s Sarcoma-Associated Herpesvirus activate lytic replication through triggering differentiation signaling

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Virus-like vesicles of Kaposi’s Sarcoma-Associated Herpesvirus activate lytic replication through triggering differentiation signaling (microRNA)

Project description:Virus-like vesicles of Kaposi’s Sarcoma-Associated Herpesvirus activate lytic replication through triggering differentiation signaling (microRNA)

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Virus-like vesicles of Kaposi’s Sarcoma-Associated Herpesvirus activate lytic replication through triggering differentiation signaling (mRNA)

Project description:Virus-like vesicles of Kaposi’s Sarcoma-Associated Herpesvirus activate lytic replication through triggering differentiation signaling (mRNA)

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Kaposi’s sarcoma-associated herpesvirus modulates the pseudouridine pathway to enhance lytic replication

Project description:Pseudouridylation is a prevalent RNA modification shown to occur in tRNAs, rRNAs, snoRNAs and most recently mRNAs and ncRNAs. Emerging evidence suggests that this dynamic RNA modification is implicated in altering gene expression by regulating RNA stability, modulating translation elongation and modifying amino acid substitution rates. However, the role of pseudouridylation in infection is poorly understood. Here we demonstrate that Kaposi’s sarcoma-associated herpesvirus (KSHV) manipulates the pseudouriylation pathway to enhance replication. We show the pseudouridine synthases (PUS), PUS1 and PUS7 are essential for efficient KSHV lytic replication, supported by the redistribution of PUS7 to viral replication and transcription complexes. Here we present a comprehensive analysis of KSHV RNA pseudouridylation revealing hundreds of modified RNAs at single-nucleotide resolution. Notably, we further demonstrate that pseudouridylation of the KSHV-encoded polyadenylated nuclear RNA (PAN) plays a significant role in the stability of PAN RNA and in the association of the KSHV ORF57 protein. Our findings reveal a novel and essential role of pseudouridine modification in the KSHV replication cycle.

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The Kaposi’s sarcoma-associated herpesvirus ORF11 protein interacts with pre-ribosome complexes during lytic replication

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