Expression data from human cell line infected by human cytomegalovirus with over-expression lncRNA
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE73954 | GEO | 2016/03/01
SECONDARY ACCESSION(S): PRJNA298579
REPOSITORIES: GEO
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Project description:We have established that human cytomegalovirus (HCMV) infection modulates the biology of target primary blood monocytes, allowing HCMV to use monocytes as 'vehicles' for its systemic spread. HCMV infection of monocytes results in rapid induction of PI(3)K and NF-kB activity. Integrins, which are upstream of the PI(3)K and NF-kB pathways, were shown to be involved in HCMV binding to and entry into fibroblasts, suggesting that receptor-ligand-mediated signaling following viral binding to integrins on monocytes could trigger the functional changes seen in infected monocytes. We now show that integrin engagement and the activation of the integrin/Src-signaling pathway is essential for the induction of HCMV-infected monocyte motility. To investigate how integrin engagement by HCMV triggers monocyte motility, we examined the infected monocyte transcriptome and found that the integrin/Src-signaling pathway regulates the expression of paxillin, which is an important signal transducer in the regulation of actin rearrangement during cell adhesion and movement. Functionally, we observed that paxillin is activated via the integrin/Src-signaling pathway and is required for monocyte motility. Because motility is intimately connected to cellular cytoskeletal organization, a process that is also important in viral entry, we investigated the role paxillin regulation plays in the process of viral entry of monocytes. New results confirmed that HCMV`s ability to enter target monocytes is significantly inhibited in cells deficient in paxillin expression or that had their integrin/Src/paxillin signaling pathway blocked. From our data, HCMV-cell interactions emerge as an essential trigger for the cellular changes that allow for HCMV entry and hematogenous dissemination. Monocytes were mock-infected, HCMV-infected, or pretreated with PP2 inhibitor prior to HCMV infection. There were three samples analyzed per individual replicate. Three replicates are included. comparative studies with a use of the specific Src kinase activity inhibitor
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Project description:Viruses are known for their extremely compact genomes composed almost entirely of protein-coding genes. Nonetheless, four long noncoding RNAs (lncRNAs) are encoded by human cytomegalovirus (HCMV). Although these RNAs accumulate to high levels during lytic infection, their functions remain largely unknown. Here, we show that HCMV-encoded lncRNA4.9 localizes to the viral nuclear replication compartment, and that its depletion restricts viral DNA replication and viral growth. RNA4.9 is transcribed from the HCMV origin of replication (oriLyt) and forms an RNA-DNA hybrid (R-loop) through its G+C-rich 5’ end, and this may be important for the initiation of viral DNA replication. Furthermore, interference with RNA4.9 expression drastically reduces the levels of the viral single-stranded DNA-binding protein (ssDBP), and overexpression of ssDBP alleviates the inhibition of viral DNA replication and growth caused by RNA4.9 depletion. We also identified a similar, oriLyt-embedded, G+C-rich lncRNA in murine cytomegalovirus (MCMV). Knockdown of this lncRNA interferes with MCMV ssDBP expression and viral DNA replication. These results indicate that HCMV RNA4.9 plays an important role in regulating viral DNA replication by coupling oriLyt activity to ssDBP levels, and that this novel activity may be conserved in other betaherpesviruses.
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