Optimized viral dose and transient immunosuppression enable herpes simplex virus ICP0-null mutants To establish wild-type levels of latency in vivo.
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Herpes simplex virus 2 ICP0 mutant viruses are avirulent and immunogenic: implications for a genital herpes vaccineFunctional interaction between class II histone deacetylases and ICP0 of herpes simplex virus type 1Re-evaluating the role of natural killer cells in innate resistance to herpes simplex virus type 1HSV-1 ICP0: paving the way for viral replicationPersistence of West Nile virus in the central nervous system and periphery of miceOcular and neural distribution of feline herpesvirus-1 during active and latent experimental infection in cats.Altered expression of antiviral cytokine mRNAs associated with cyclophosphamide's enhancement of viral oncolysisICP0 is required for efficient reactivation of herpes simplex virus type 1 from neuronal latency.ICP0, ICP4, or VP16 expressed from adenovirus vectors induces reactivation of latent herpes simplex virus type 1 in primary cultures of latently infected trigeminal ganglion cells.The dominant-negative herpes simplex virus type 1 (HSV-1) recombinant CJ83193 can serve as an effective vaccine against wild-type HSV-1 infection in mice.Point mutations in herpes simplex virus type 1 oriL, but not in oriS, reduce pathogenesis during acute infection of mice and impair reactivation from latency.The cyclin-dependent kinase inhibitor roscovitine inhibits the transactivating activity and alters the posttranslational modification of herpes simplex virus type 1 ICP0.Beta interferon and gamma interferon synergize to block viral DNA and virion synthesis in herpes simplex virus-infected cells.Alpha/Beta interferon and gamma interferon synergize to inhibit the replication of herpes simplex virus type 1.ICP0 is not required for efficient stress-induced reactivation of herpes simplex virus type 1 from cultured quiescently infected neuronal cells.Failure of thymidine kinase-negative herpes simplex virus to reactivate from latency following efficient establishment.Early establishment of gamma-herpesvirus latency: implications for immune control.ICP0 antagonizes Stat 1-dependent repression of herpes simplex virus: implications for the regulation of viral latency.ICP22 is required for wild-type composition and infectivity of herpes simplex virus type 1 virions.Establishment and maintenance of gammaherpesvirus latency are independent of infective dose and route of infectionHerpes simplex virus 1 ICP0 phosphorylation site mutants are attenuated for viral replication and impaired for explant-induced reactivation.Role of ICP0 in the strategy of conquest of the host cell by herpes simplex virus 1Construction and characterization of a herpes simplex virus type I recombinant expressing green fluorescent protein: acute phase replication and reactivation in miceCD4+CD25+ T cells regulate virus-specific primary and memory CD8+ T cell responses.A Herpesviral Lytic Protein Regulates the Structure of Latent Viral Chromatin.Herpes simplex virus 1 ICP22 but not US 1.5 is required for efficient acute replication in mice and VICE domain formation.Re-evaluating natural resistance to herpes simplex virus type 1.Immunosuppressive drugs modulate the replication of hepatitis B virus (HBV) in a hydrodynamic injection mouse model.Phosphorylation site mutations affect herpes simplex virus type 1 ICP0 function.Impact of Type I Interferon on the Safety and Immunogenicity of an Experimental Live-Attenuated Herpes Simplex Virus 1 Vaccine in Mice.Herpes simplex virus type 1 C-terminal variants of the origin binding protein (OBP), OBPC-1 and OBPC-2, cooperatively regulate viral DNA levels in vitro, and OBPC-2 affects mortality in mice.Role of a cdk5-associated protein, p35, in herpes simplex virus type 1 replication in vivo.Ocular reactivation phenotype of HSV-1 strain F(MP)E, a corticosteroid-sensitive strain.Development of a novel ex vivo model of corneal fungal adherence.CCCTC-Binding Factor Acts as a Heterochromatin Barrier on Herpes Simplex Viral Latent Chromatin and Contributes to Poised Latent Infection.Interaction between the cellular E3 ubiquitin ligase SIAH-1 and the viral immediate-early protein ICP0 enables efficient replication of Herpes Simplex Virus type 2 in vivoHSV-1 as a Model for Emerging Gene Delivery Vehicles
P2860
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P2860
Optimized viral dose and transient immunosuppression enable herpes simplex virus ICP0-null mutants To establish wild-type levels of latency in vivo.
description
2000 nî lūn-bûn
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2000 թուականի Յուլիսին հրատարակուած գիտական յօդուած
@hyw
2000 թվականի հուլիսին հրատարակված գիտական հոդված
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2000年の論文
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2000年論文
@yue
2000年論文
@zh-hant
2000年論文
@zh-hk
2000年論文
@zh-mo
2000年論文
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2000年论文
@wuu
name
Optimized viral dose and trans ...... ype levels of latency in vivo.
@ast
Optimized viral dose and trans ...... ype levels of latency in vivo.
@en
type
label
Optimized viral dose and trans ...... ype levels of latency in vivo.
@ast
Optimized viral dose and trans ...... ype levels of latency in vivo.
@en
prefLabel
Optimized viral dose and trans ...... ype levels of latency in vivo.
@ast
Optimized viral dose and trans ...... ype levels of latency in vivo.
@en
P2860
P1433
P1476
Optimized viral dose and trans ...... ype levels of latency in vivo.
@en
P2093
P A Schaffer
W P Halford
P2860
P304
P356
10.1128/JVI.74.13.5957-5967.2000
P577
2000-07-01T00:00:00Z