Immunization with replication-defective mutants of herpes simplex virus type 1: sites of immune intervention in pathogenesis of challenge virus infection.
about
Control of STDs--the role of prophylactic vaccines against herpes simplex virus.The cytotoxic T-cell response to herpes simplex virus type 1 infection of C57BL/6 mice is almost entirely directed against a single immunodominant determinant.Construction and properties of a herpes simplex virus 2 dl5-29 vaccine candidate strain encoding an HSV-1 virion host shutoff protein.Mucosal and parenteral vaccination against acute and latent murine cytomegalovirus (MCMV) infection by using an attenuated MCMV mutant.Immunization with a single major histocompatibility complex class I-restricted cytotoxic T-lymphocyte recognition epitope of herpes simplex virus type 2 confers protective immunity.Herpes simplex virus virion host shutoff (vhs) activity alters periocular disease in mice.Vaccine protection against simian immunodeficiency virus by recombinant strains of herpes simplex virus.Construction, phenotypic analysis, and immunogenicity of a UL5/UL29 double deletion mutant of herpes simplex virus 2.Disruption of virion host shutoff activity improves the immunogenicity and protective capacity of a replication-incompetent herpes simplex virus type 1 vaccine strain.Vaccine-induced serum immunoglobin contributes to protection from herpes simplex virus type 2 genital infection in the presence of immune T cells.Active immunization in the United States: developments over the past decade.B7 costimulation molecules encoded by replication-defective, vhs-deficient HSV-1 improve vaccine-induced protection against corneal diseaseThe 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.Herpes simplex virus vectors elicit durable immune responses in the presence of preexisting host immunity.Therapeutic immunization with a virion host shutoff-defective, replication-incompetent herpes simplex virus type 1 strain limits recurrent herpetic ocular infectionMechanism of reduced T-cell effector functions and class-switched antibody responses to herpes simplex virus type 2 in the absence of B7 costimulationRegulation of herpes simplex virus gamma(1)34.5 expression and oncolysis of diffuse liver metastases by Myb34.5.Pathogenesis of herpes simplex virus type 2 virion host shutoff (vhs) mutants.Absence or overexpression of the Varicella-Zoster Virus (VZV) ORF29 latency-associated protein impairs late gene expression and reduces VZV latency in a rodent modelAbility of herpes simplex virus vectors to boost immune responses to DNA vectors and to protect against challenge by simian immunodeficiency virusProtease-deficient herpes simplex virus protects mice from lethal herpesvirus infection.Immunization with a replication-deficient mutant of herpes simplex virus type 1 (HSV-1) induces a CD8+ cytotoxic T-lymphocyte response and confers a level of protection comparable to that of wild-type HSV-1Immunization with a replication-defective herpes simplex virus 2 mutant reduces herpes simplex virus 1 infection and prevents ocular disease.Immunization against genital herpes with a vaccine virus that has defects in productive and latent infection.BAC-VAC, a novel generation of (DNA) vaccines: A bacterial artificial chromosome (BAC) containing a replication-competent, packaging-defective virus genome induces protective immunity against herpes simplex virus 1.Enhanced pathogenesis of an attenuated herpes simplex virus for mice lacking Stat1HSV-1 strain McKrae is more neuroinvasive than HSV-1 KOS after corneal or vaginal inoculation in miceHost responses to wild-type and attenuated herpes simplex virus infection in the absence of Stat1High-level expression of glycoprotein D by a dominant-negative HSV-1 virus augments its efficacy as a vaccine against HSV-1 infection.Prevention of genital herpes simplex virus type 1 and 2 disease in mice immunized with a gD-expressing dominant-negative recombinant HSV-1.Herpes simplex virus as a tool to define the role of complement in the immune response to peripheral infection.Effective vaccination against long-term gammaherpesvirus latency.Viral replication is required for induction of ocular immunopathology by herpes simplex virus.Analysis of Herpes Simplex Virus Reactivation in Explant Reveals a Method-Dependent Difference in Measured Timing of Reactivation.Critical role of CD4 T cells in an antibody-independent mechanism of vaccination against gammaherpesvirus latency.Optimal long-term humoral responses to replication-defective herpes simplex virus require CD21/CD35 complement receptor expression on stromal cells.
P2860
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P2860
Immunization with replication-defective mutants of herpes simplex virus type 1: sites of immune intervention in pathogenesis of challenge virus infection.
description
1994 nî lūn-bûn
@nan
1994年の論文
@ja
1994年論文
@yue
1994年論文
@zh-hant
1994年論文
@zh-hk
1994年論文
@zh-mo
1994年論文
@zh-tw
1994年论文
@wuu
1994年论文
@zh
1994年论文
@zh-cn
name
Immunization with replication- ...... of challenge virus infection.
@ast
Immunization with replication- ...... of challenge virus infection.
@en
type
label
Immunization with replication- ...... of challenge virus infection.
@ast
Immunization with replication- ...... of challenge virus infection.
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prefLabel
Immunization with replication- ...... of challenge virus infection.
@ast
Immunization with replication- ...... of challenge virus infection.
@en
P2860
P1433
P1476
Immunization with replication- ...... s of challenge virus infection
@en
P2093
L A Morrison
P2860
P304
P407
P577
1994-02-01T00:00:00Z