Daniel Gonzalez-Dunia

1-beta-D-arabinofuranosylcytosine inhibits borna disease virus replication and spread.

Borna disease virus glycoprotein is required for viral dissemination in neurons.

Persistent, noncytolytic infection of neurons by Borna disease virus interferes with ERK 1/2 signaling and abrogates BDNF-induced synaptogenesis.

2'-fluoro-2'-deoxycytidine inhibits Borna disease virus replication and spread.

Identification of a novel natural regulatory CD8 T-cell subset and analysis of its mechanism of regulation.

Functional and genetic analysis of two CD8 T cell subsets defined by the level of CD45RC expression in the rat.

Mechanism of the antiviral action of 1-beta-D-arabinofuranosylcytosine on Borna disease virus.

Borna disease virus interference with neuronal plasticity.

Borna disease virus blocks potentiation of presynaptic activity through inhibition of protein kinase C signaling.

Pertussis toxin reduces the number of splenic Foxp3+ regulatory T cells.

Anaplastic lymphoma kinase is a dependence receptor whose proapoptotic functions are activated by caspase cleavage.

Tracking antigen-specific CD8+ T cells in the rat using MHC class I multimers.

Borna disease virus infection impairs synaptic plasticity.

High reproducibility of two-dimensional liquid chromatography using pH-driven fractionation with a pressure-resistant electrode.

Proteomic analysis reveals selective impediment of neuronal remodeling upon Borna disease virus infection.

Mutation of the protein kinase C site in borna disease virus phosphoprotein abrogates viral interference with neuronal signaling and restores normal synaptic activity.

Protein kinase C-dependent phosphorylation of Borna disease virus P protein is required for efficient viral spread.

Neurons are MHC class I-dependent targets for CD8 T cells upon neurotropic viral infection.

Neurons as targets for T cells in the nervous system.

Analysis of borna disease virus trafficking in live infected cells by using a virus encoding a tetracysteine-tagged p protein.