03). These data suggest that transmission or early HLA-driven selection of Gag polymorphisms results in reduced early cytotoxic T-lymphocyte (CTL) responses and higher viral load set

points. In support of the former, 46% of individuals with nonprotective alleles harbored a Gag polymorphism exclusively associated with a protective HLA allele, see more indicating a high rate of their transmission in sub-Saharan Africa. Overall, HIV disease progression is likely to be affected by the ability to mount effective Gag CTL responses as well as the replication capacity of the transmitted virus.”
“Musical training strengthens speech perception in the presence of background noise. Given that the ability to make use of speech sound regularities, such as pitch, underlies perceptual acuity in challenging listening environments, we asked whether musicians’ enhanced speech-in-noise perception is facilitated by increased neural sensitivity

to acoustic regularities. To this aim we examined subcortical encoding of the same speech syllable presented in predictable and variable conditions and speech-in-noise perception in 31 musicians and nonmusicians. We anticipated that musicians would demonstrate greater neural enhancement of speech presented in the predictable compared to the variable condition than nonmusicians. Accordingly, musicians demonstrated more robust neural encoding of the fundamental frequency (i.e., pitch)

of speech presented in the predictable relative to the variable condition than nonmusicians. The degree of neural enhancement observed Bindarit to predictable speech correlated with subjects’ musical practice histories as well as with their speech-in-noise perceptual abilities. Taken together, our findings suggest that subcortical sensitivity to speech regularities is shaped by musical training and may contribute to musicians’ enhanced speech-in-noise perception. (C) 2011 Elsevier Ltd. those All rights reserved.”
“Human parainfluenza virus type 2 (HPIV-2), an important pediatric respiratory pathogen, encodes a V protein that inhibits type I interferon (IFN) induction and signaling. Using reverse genetics, we attempted the recovery of a panel of V mutant viruses that individually contained one of six cysteine-to-serine (residues 193, 197, 209, 211, 214, and 218) substitutions, one of two paired charge-to-alanine (R175A/R176A and R205A/K206A) substitutions, or a histidine-to-phenylalanine (H174F) substitution. This mutagenesis was performed using a cDNA-derived HPIV-2 virus that expressed the V and P coding sequences from separate mRNAs. Of the cysteine substitutions, only C193S, C214S, and C218S yielded viable virus, and only the C214S mutant replicated well enough for further analysis. The H174F, R175A/R176A, and R205A/K206A mutants were viable and replicated well.