The DNase of gammaherpesviruses impairs recognition by virus-specific CD8+ T cells through an additional host shutoff function.
about
Shutoff of Host Gene Expression in Influenza A Virus and Herpesviruses: Similar Mechanisms and Common ThemesUnderstanding the interplay between host immunity and Epstein-Barr virus in NPC patientsThe interplay between Epstein-Barr virus and B lymphocytes: implications for infection, immunity, and diseaseKSHV: pathways to tumorigenesis and persistent infectionCrystal structure of the shutoff and exonuclease protein from the oncogenic Kaposi's sarcoma-associated herpesvirusCrystal structure of a KSHV-SOX-DNA complex: insights into the molecular mechanisms underlying DNase activity and host shutoffViral inhibition of the transporter associated with antigen processing (TAP): a striking example of functional convergent evolutionAberrant herpesvirus-induced polyadenylation correlates with cellular messenger RNA destruction.The Epstein-Barr virus G-protein-coupled receptor contributes to immune evasion by targeting MHC class I molecules for degradationStage-specific inhibition of MHC class I presentation by the Epstein-Barr virus BNLF2a protein during virus lytic cycle.Epstein-Barr virus DNase (BGLF5) induces genomic instability in human epithelial cells.Humoral immune responses to Epstein-Barr virus encoded tumor associated proteins and their putative extracellular domains in nasopharyngeal carcinoma patients and regional controls.Deep sequencing reveals direct targets of gammaherpesvirus-induced mRNA decay and suggests that multiple mechanisms govern cellular transcript escape.Global mRNA degradation during lytic gammaherpesvirus infection contributes to establishment of viral latency.Kaposi's sarcoma-associated herpesvirus K3 and K5 ubiquitin E3 ligases have stage-specific immune evasion roles during lytic replicationEpstein-Barr virus evades CD4+ T cell responses in lytic cycle through BZLF1-mediated downregulation of CD74 and the cooperation of vBcl-2.The EBV immunoevasins vIL-10 and BNLF2a protect newly infected B cells from immune recognition and eliminationImmune escape of γ-herpesviruses from adaptive immunityPML nuclear bodies and SATB1 are associated with HLA class I expression in EBV+ Hodgkin lymphomaEpstein-Barr virus transcription factor Zta acts through distal regulatory elements to directly control cellular gene expression.Persistent infection drives the development of CD8+ T cells specific for late lytic infection antigens in lymphocryptovirus-infected macaques and Epstein-Barr virus-infected humans.Latent Membrane Protein LMP2A Impairs Recognition of EBV-Infected Cells by CD8+ T Cells.The "Bridge" in the Epstein-Barr virus alkaline exonuclease protein BGLF5 contributes to shutoff activity during productive infection.Hiding lipid presentation: viral interference with CD1d-restricted invariant natural killer T (iNKT) cell activationEBV BILF1 evolved to downregulate cell surface display of a wide range of HLA class I molecules through their cytoplasmic tail.Host shutoff is a conserved phenotype of gammaherpesvirus infection and is orchestrated exclusively from the cytoplasm.Epstein-Barr virus, rapamycin, and host immune responses.Epstein-Barr virus microRNAs reduce immune surveillance by virus-specific CD8+ T cells.The Epstein-Barr virus protein kinase BGLF4 and the exonuclease BGLF5 have opposite effects on the regulation of viral protein production.Gammaherpesviral gene expression and virion composition are broadly controlled by accelerated mRNA degradation.Immune responses to Epstein-Barr virus: molecular interactions in the virus evasion of CD8+ T cell immunityProspects of a novel vaccination strategy for human gamma-herpesviruses.Exploiting human herpesvirus immune evasion for therapeutic gain: potential and pitfalls.Epstein-Barr virus genetics: talking about the BAC generation.Herpesviruses placating the unwilling host: manipulation of the MHC class II antigen presentation pathway.Dynamic Epstein-Barr virus gene expression on the path to B-cell transformation.Emerging roles for RNA degradation in viral replication and antiviral defense.The Missing Link in Epstein-Barr Virus Immune Evasion: the BDLF3 Gene Induces Ubiquitination and Downregulation of Major Histocompatibility Complex Class I (MHC-I) and MHC-IIThe Epstein-Barr virus-encoded BILF1 protein modulates immune recognition of endogenously processed antigen by targeting major histocompatibility complex class I molecules trafficking on both the exocytic and endocytic pathwaysThe Epstein-Barr virus alkaline exonuclease BGLF5 serves pleiotropic functions in virus replication.
P2860
Q26752361-7D70DB5E-6383-4F61-82CC-11B22508B35CQ26823898-9406484E-8758-4118-9747-6B28A6EEB5F8Q26998401-7F6F0C94-EEF0-4A2B-98C9-6E7D84BFB39EQ27026000-9D8783CD-D5B4-43ED-8ABA-2088A46688C6Q27657862-0CDCD706-27CF-4CC0-A9D9-9523BEC3D4E9Q27667301-C98337C5-52FE-4AF8-80EA-78F7C1012950Q28083232-70D148D0-D04B-41B5-A76B-98598737DB74Q30863867-C5A712FF-0ED3-4731-B0CE-52B5C94625D3Q33396983-EE81EF29-FA5B-4064-8069-86723BBADFD1Q33474804-BEAA1E4B-7913-4CD0-B8CA-9C5121DC1C5AQ33760239-82FAC838-E17D-4395-A22F-50B137DFD9AEQ33822681-50358E11-C964-4233-83B3-2C4E395E7DF8Q33900385-ADE842CC-818B-4C7F-BA34-60F5EA26BAE3Q33979518-8D217171-58E8-45BF-8DBE-71582944CDAFQ34059252-94C0D9ED-2AF4-43AA-A622-BA96E2291635Q34116845-FE0D406D-1353-4F3F-B0A5-4DEB3E2D5138Q34277034-A4EBC99B-C916-4152-8341-59CF8E42A1A4Q34345549-E24CC642-98CA-4FBE-8C03-035EB35C15B6Q34979670-43397343-D2D1-4AF7-9BF7-6CD110773DAEQ35476446-5502BF3F-D3BF-4D88-9D1D-DFAA8C0B4AB2Q35531669-DD804587-EA00-442B-87F8-41FA214C5BC4Q35661383-5F7127CD-1C9D-419B-AF15-E2DBAA3969C0Q36154936-2DAB3656-14F1-461A-973E-AF5C11323E18Q36395876-F7C10F4A-39C9-4FF1-8262-4D68308C773BQ36590231-20770EB7-B23A-448F-A079-4151717A4DA9Q37333940-30FDF967-9F76-4BA0-988B-DC44476C439DQ37342546-254DE17B-FF7E-4CC6-8FED-46154F9027E0Q37369220-B3A488CE-5420-484A-A2A3-7B7809B1C97AQ37410869-AED1758C-3BEE-4431-8151-87A3AF438565Q37488124-8A25DEE6-C80D-4CEC-B1A6-78045E7A2E90Q37652046-7534E015-14B2-4FE3-841E-F99EF07972F0Q37780705-D4548872-A649-41FF-9BA4-7601A43C9583Q37837495-AD55B451-90DC-4042-9CF5-08BD213ABAFDQ37856451-DBFE720E-74C0-4F05-81FA-E0AEAFA213B9Q38046606-B3116948-3104-4279-90BF-F7F4ADD5FDDDQ38174306-C6A1AC19-2521-4972-856A-F69AFDD664FAQ38365673-17BD8676-AAA5-46C0-913E-44C05D25BB3BQ38827812-AD130F74-89C1-4CE7-BF22-4D86F136E757Q39625133-E38B0B2C-895D-407A-9295-FA2CF2BE7BA3Q39876597-F60DB444-DC19-483F-93D5-B6712F3720D6
P2860
The DNase of gammaherpesviruses impairs recognition by virus-specific CD8+ T cells through an additional host shutoff function.
description
2007 nî lūn-bûn
@nan
2007年の論文
@ja
2007年論文
@yue
2007年論文
@zh-hant
2007年論文
@zh-hk
2007年論文
@zh-mo
2007年論文
@zh-tw
2007年论文
@wuu
2007年论文
@zh
2007年论文
@zh-cn
name
The DNase of gammaherpesviruse ...... itional host shutoff function.
@en
type
label
The DNase of gammaherpesviruse ...... itional host shutoff function.
@en
prefLabel
The DNase of gammaherpesviruse ...... itional host shutoff function.
@en
P2093
P2860
P356
P1433
P1476
The DNase of gammaherpesviruse ...... itional host shutoff function.
@en
P2093
Daphne van Leeuwen
Emmanuel J H J Wiertz
Jaap M Middeldorp
Maaike E Ressing
Wendy Thomas
P2860
P304
P356
10.1128/JVI.01946-07
P407
P577
2007-12-19T00:00:00Z