Ex vivo stimulation of B cells latently infected with gammaherpesvirus 68 triggers reactivation from latency
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T cell memory in the context of persistent herpes viral infectionsInterplay of Murine Gammaherpesvirus 68 with NF-kappaB Signaling of the HostViral cyclins mediate separate phases of infection by integrating functions of distinct mammalian cyclinsRTA promoter demethylation and histone acetylation regulation of murine gammaherpesvirus 68 reactivationThe murine gammaherpesvirus 68 M2 gene is required for efficient reactivation from latently infected B cells.Role of B-cell proliferation in the establishment of gammaherpesvirus latency.Global mRNA degradation during lytic gammaherpesvirus infection contributes to establishment of viral latency.The viral latency-associated nuclear antigen augments the B-cell response to antigen in vivo3,4-Methylenedioxymethamphetamine (MDMA) alters acute gammaherpesvirus burden and limits interleukin 27 responses in a mouse model of viral infection.In vivo activation of toll-like receptor-9 induces an age-dependent abortive lytic cycle reactivation of murine gammaherpesvirus-68.Evidence for CDK-dependent and CDK-independent functions of the murine gammaherpesvirus 68 v-cyclin.Exacerbated metastatic disease in a mouse mammary tumor model following latent gammaherpesvirus infection.Establishment of B-cell lines latently infected with reactivation-competent murine gammaherpesvirus 68 provides evidence for viral alteration of a DNA damage-signaling cascade.Efficient infection of a human B cell line with cell-free Kaposi's sarcoma-associated herpesvirus.Is murine gammaherpesvirus-68 (MHV-68) a suitable immunotoxicological model for examining immunomodulatory drug-associated viral recrudescence?Activation of the B cell antigen receptor triggers reactivation of latent Kaposi's sarcoma-associated herpesvirus in B cells.De novo infection of B cells during murine gammaherpesvirus 68 latencyRTA Occupancy of the Origin of Lytic Replication during Murine Gammaherpesvirus 68 Reactivation from B Cell Latency.Murine gammaherpesvirus 68 reactivation from B cells requires IRF4 but not XBP-1.Blimp-1-dependent plasma cell differentiation is required for efficient maintenance of murine gammaherpesvirus latency and antiviral antibody responses.Signaling through Toll-like receptors induces murine gammaherpesvirus 68 reactivation in vivo.Regulation of gammaherpesvirus lytic replication by endoplasmic reticulum stress-induced transcription factors ATF4 and CHOP.
P2860
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P2860
Ex vivo stimulation of B cells latently infected with gammaherpesvirus 68 triggers reactivation from latency
description
2005 nî lūn-bûn
@nan
2005 թուականի Ապրիլին հրատարակուած գիտական յօդուած
@hyw
2005 թվականի ապրիլին հրատարակված գիտական հոդված
@hy
2005年の論文
@ja
2005年論文
@yue
2005年論文
@zh-hant
2005年論文
@zh-hk
2005年論文
@zh-mo
2005年論文
@zh-tw
2005年论文
@wuu
name
Ex vivo stimulation of B cells ...... gers reactivation from latency
@ast
Ex vivo stimulation of B cells ...... gers reactivation from latency
@en
type
label
Ex vivo stimulation of B cells ...... gers reactivation from latency
@ast
Ex vivo stimulation of B cells ...... gers reactivation from latency
@en
prefLabel
Ex vivo stimulation of B cells ...... gers reactivation from latency
@ast
Ex vivo stimulation of B cells ...... gers reactivation from latency
@en
P2093
P2860
P1433
P1476
Ex vivo stimulation of B cells ...... gers reactivation from latency
@en
P2093
Janice M Moser
Jason W Upton
Kathleen S Gray
Samuel H Speck
P2860
P304
P356
10.1128/JVI.79.8.5227-5231.2005
P577
2005-04-01T00:00:00Z