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“Matrix (M) protein mutants of vesicular stomatitis virus (VSV), such as rM51R-M virus, are less virulent than wild-type (wt) VSV strains due to their inability to
suppress innate immunity. Studies presented here show that when inoculated intranasally into mice, rM51R-M virus was cleared from nasal mucosa by day 2 postinfection and was attenuated for spread to the central nervous system, in contrast to wt VSV, thus accounting for its reduced virulence. However, it stimulated an antibody response similar to that in mice infected with the wt virus, indicating that it has the ability to induce adaptive immunity in vivo without causing disease. These results support the use of M protein mutants of VSV selleck chemicals Torin 1 manufacturer as vaccine vectors.”
“Ethanol exerts effects on the brain noradrenergic system, and these are thought to contribute to the sedative/hypnotic (depressant) effects of ethanol. Recent studies suggest that the norepinephrine transporter (NET) plays an important role in modulating ethanol’s depressant effects. The aim of the present study was to further characterize this role. Transporter blockers with varying affinity for NET versus the serotonin
transporter (desipramine > fluoxetine > citalopram) were tested for their ability to alter ethanol’s depressant effects, and for comparison, hypothermic effects. Effects of desipramine on another depressant, pentobarbital, were examined. Desipramine potentiation of ethanol’s depressant effects was assessed following depletion of brain
norepinephrine via N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine hydrochloride (DSPA) treatment, or depletion of brain 5-HT via para-chlorophenylalanine methyl ester hydrochloride (PCPA) treatment. The effects of co-administration of either the selective alpha 2-adrenoreceptor agonist (dexmedetomidine) or the selective alpha 2-adrenoreceptor antagonist (atipamezole) on desipramine’s effect on ethanol’s depressant effects were examined. Given the close link between stress, ethanol and norepinephrine, desipramine potentiation of ethanol’s depressant effects was tested following repeated forced swim stress. Results showed that desipramine, but not SERT-selective doses of citalopram or fluoxetine, strongly potentiated the depressant (not hypothermic) effects of ethanol. These effects were mimicked by dexmedetomidine Glycogen branching enzyme and blocked by atipamezole, but not by depletion of either norepinephrine or 5-HT. Desipramine potentiation of ethanol’s depressant effects was abolished following repeated stress. Present findings further support a major role for NET and the alpha 2-adrenoreceptor in modulating the depressant effects of ethanol, with possible implications for understanding the role of noradrenergic dysfunction in stress-related alcoholism. Published by Elsevier Ltd.”
“VP22, encoded by the UL49 gene of Marek’s disease virus (MDV), is indispensable for virus cell-to-cell spreading.