Relationship between Virucidal Efficacy and Free Iodine Concentration of Povidone-Iodine in Buffer Solution.

Povidone-iodine solutions prepared to various concentrations (0.01, 0.1, 1 and 10%) with 0.2M phosphate buffer (pH 7.0) (PVP-I PB) were analyzed to determine their free iodine concentrations using membrane permeation cells, and their inactivation effects on three viruses (influenza A virus, poliovirus type 1 and adenovirus type 3) were examined. The free iodine concentrations in the 0.01-10% PVP-I PB were determined to be 1.84, 4.88, 1.58 and 0.17 ppm (approximate values), respectively, with the maximum obtained for the 0.1% solution. The virucidal efficacy of these PVP-I PB against poliovirus type 1 and adenovirus type 3 was found to be generally dependent on free iodine concentration, with the 0.1% solution being the most effective. Influenza A virus was inactivated with an action time of 15 s at all four concentrations examined. The results of this study suggested an association between free iodine concentration and virucidal efficacy for the 0.01-10% PVP-I PB.

Sugar-responsive gene expression and the agr system are required for colony spreading in Staphylococcus aureus.

Staphylococcus aureus spreads on soft agar surfaces, which is called "colony spreading". Here, we report that the colony spreading in S. aureus was promoted by the addition of glucose to soft agar plates. Disruption of ccpA and hprK, which are involved in catabolite repression, decreased the colony spreading ability promoted by glucose. Deletion of the agr locus, a virulence regulatory element whose expression is activated by glucose in a ccpA-dependent manner, abolished the colony spreading promoted by glucose. Disruption of clpP and arlRS, which contributes to agr expression, also decreased glucose-promoted colony spreading. These findings suggest that S. aureus colony spreading requires the expression of agr, which is positively regulated by environmental carbon sources, and that virulence gene expression and colony spreading induced by agr are simultaneously activated in the S. aureus infectious process.

Novel RNA polymerase II mutation suppresses transcriptional fidelity and oxidative stress sensitivity in rpb9Delta yeast.

We previously reported that transcription elongation factor S-II and RNA polymerase II subunit Rpb9 maintain transcriptional fidelity and contribute to oxidative stress resistance in yeast. Here we examined whether other transcription elongation-related factors affect transcriptional fidelity in vivo. Among the 17 mutants of transcription elongation-related factors analyzed, most were not responsible for maintaining transcriptional fidelity. This finding indicates that transcriptional fidelity is controlled by a limited number of transcription elongation-related factors including S-II and Rpb9 and not by all transcription elongation-related factors. In contrast, by screening rpb9Delta cell revertants for sensitivity to the oxidant menadione, we identified a novel mutation in RNA polymerase II, rpb1-G730D, which suppressed both reduced transcriptional fidelity and oxidative stress sensitivity. These findings suggest that the maintenance of transcriptional fidelity that is mediated by transcription machinery directly confers oxidative stress resistance.