herpes simplex/albumin

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The virucidal EB peptide protects host cells from herpes simplex virus type 1 infection in the presence of serum albumin and aggregates proteins in a detergent-like manner.

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The linear cationic amphiphilic EB peptide, derived from the FGF4 signal sequence, was previously shown to be virucidal and to block herpes simplex type I (HSV-1) entry (H. Bultmann, J. S. Busse, and C. R. Brandt, J. Virol. 75:2634-2645, 2001). Here we show that cells treated with EB

Hepatoma-specific antitumor activity of an albumin enhancer/promoter regulated herpes simplex virus in vivo.

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Targeting viral vectors to appropriate cell types so that normal cells are not adversely affected is an important goal for gene therapy. Previously, we described a novel approach to viral gene therapy using a conditional, replication-competent herpes simplex virus (HSV), where replication and

Cerebrospinal fluid immunoglobulin G and albumin dynamics. A comparison in experimental allergic encephalitis and herpes simplex encephalitis in rabbits.

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First description of single-pass albumin dialysis combined with cytokine adsorption in fulminant liver failure and hemophagocytic syndrome resulting from generalized herpes simplex virus 1 infection.

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Acute and latent herpes simplex virus neurological disease in mice immunized with purified virus-specific glycoproteins gB or gD.

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Groups of 5-week-old BALB/c mice were immunized intraperitoneally with approximately 10 micrograms of purified alum-precipitated glycoprotein gB or gD of either herpes simplex virus type 1 (HSV-1) or type 2 (HSV-2) origin. Control mice received injections of alum-precipitated 1% bovine serum albumin

[Chronic herpes simplex encephalitis initially presenting with persistent myoclonus].

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A 59-year-old female patient with atypical chronic herpes simplex encephalitis was reported. Initial symptom was persistent myoclonus involving the trunk and limb muscles, and later lateral gaze palsy to the left side, cerebellar ataxia, consciousness disturbance and other brainstem symptoms

Herpes simplex virus encephalitis. Prolonged intrathecal IgG synthesis and cellular activity in the cerebrospinal fluid with transient impairment of blood-brain barrier.

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Alterations of cerebrospinal fluid (CFS) proteins and cells and blood-brain barrier impairment were determined in 4 patients with proven and 2 patients with presumptive herpes simplex virus encephalitis ( HSVE ) using simultaneous nephelometric measurements of CSF and serum albumin and

Virus neutralizing activity induced by synthetic peptides of glycoprotein D of herpes simplex virus type 1, selected by their reactivity with hyperimmune sera from mice.

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Mice were immunized with synthetic peptides covering the first 56 amino acids of herpes simplex virus type 1 (HSV-1) glycoprotein D (gD) and a fusion protein, produced in Escherichia coli, containing the first 55 amino acid residues of gD. It was found that mice immunized with peptides composed of

Role of mannose-6-phosphate receptors in herpes simplex virus entry into cells and cell-to-cell transmission.

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Herpes simplex virus (HSV) glycoprotein D (gD) is essential for virus entry into cells, is modified with mannose-6-phosphate (M-6-P), and binds to both the 275-kDa M-6-P receptor (MPR) and the 46-kDa MPR (C. R. Brunetti, R. L. Burke, S. Kornfeld, W. Gregory, K. S. Dingwell, F. Masiarz, and D. C.

Reduced herpes simplex virus type 1 latency in Flt-3 ligand-treated mice is associated with enhanced numbers of natural killer and dendritic cells.

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We have investigated the effect of Flt-3 ligand (Flt-3L) on the resistance to herpes simplex virus type-1 (HSV-1) infection in BALB/c mice which are normally highly susceptible to challenge with this virus. We have confirmed data by others that in vivo treatment with Flt-3L causes an increase in

Time course of chemokines in the cerebrospinal fluid and serum during herpes simplex type 1 encephalitis.

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Chemokines (chemoattractant cytokines) attract and activate specific leukocyte subsets. With regard to their expression by brain parenchymal cells, they may represent the key molecules that control leukocyte entry into the subarachnoid space. In order to evaluate the contribution of chemokines in

Herpes simplex virus phosphoproteins. II. Characterization of the virion protein kinase and of the polypeptides phosphorylated in the virion.

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The protein kinase associated with purified herpes simplex virus 1 and 2 virions partitioned with the capsid-tegument structures and was not solubilized by non-ionic detergents and low, non-inhibitory concentrations of urea. The enzyme required Mg2+ or Mn2+ and utilized ATP or GTP. The activity was

Adjuvant-independent enhanced immune responses to recombinant herpes simplex virus type 1 glycoprotein D by fusion with biologically active interleukin-2.

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A truncated herpes simplex virus (HSV) type 1 glycoprotein D (t-gD) gene was fused to the human interleukin-2 (IL-2) gene (t-gD-IL-2 gene) and introduced into mouse myeloma Sp2/0 cells. The gene product, t-gD-IL-2, secreted from the cells was immunoprecipitated with five monoclonal antibodies

Antibodies to a synthetic oligopeptide that react with herpes simplex virus type 1 and 2 glycoprotein C.

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Nucleotide sequence and mRNA localization studies have allowed the prediction of the amino acid sequence of herpes simplex virus type 1 (HSV-1) glycoprotein C (gC). We immunized a rabbit with a conjugate of bovine serum albumin and a synthetic peptide having the same sequence as that deduced for

The influence of different adjuvants on the immune response to a synthetic peptide comprising amino acid residues 9-21 of herpes simplex virus type 1 glycoprotein D.

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The immuno-modulating properties of different adjuvant systems on the murine humoral and cellular immune response to a synthetic peptide comprising amino acid residues 9-21 of glycoprotein D of herpes simplex virus type 1 (HSV-1) were investigated. For immunization, the peptide was conjugated to

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