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“As part of an ongoing study of early human immunodeficiency virus type 1 (HIV-1) infection in sub-Saharan African countries, we have identified 134 seroconverters (SCs) with distinct acute-phase (peak) and early chronic-phase (set-point) viremias. SCs with class I human leukocyte antigen (HLA) variants B*44 and B*57 had much lower peak viral loads (VLs) than SCs without these variants (adjusted linear regression beta values of -1.08 +/- 0.26 log(10) [mean +/- standard error] and -0.83 +/- 0.27 log(10), respectively; P < 0.005 for both), after accounting for several nongenetic factors, including gender, age at estimated date

of infection, duration of infection, and country of origin. These findings were confirmed by alternative models in which major viral subtypes (A1, C, and others) in the Blasticidin S supplier same SCs replaced country of origin as a covariate (P <= 0.03). see more Both B*44 and B*57 were also highly favorable (P <= 0.03) in analyses of set-point VLs. Moreover, B*44 was associated with relatively high CD4(+) T-cell counts during early chronic infection (P = 0.02). Thus, at least two common HLA-B variants showed strong influences on acute-phase

as well as early chronic-phase VL, regardless of the infecting viral subtype. If confirmed, the identification of B*44 as another favorable marker in primary HIV-1 infection should help dissect mechanisms of early immune protection against HIV-1 infection.”
“Methylisothiazolinone (MIT) is a commonly used biocide known to be neurotoxic in vitro. Brief exposure of cortical neurons in culture to MIT results in increased

neurodegeneration, whereas chronic exposure of developing neurons in culture to low concentrations of MIT has been shown to interfere with normal neurite outgrowth. However, the effects of chronic MIT exposure on the developing nervous system have not been tested in vivo. Here we expose Xenopus laevis tadpoles to sub-lethal concentrations of MIT during a critical period in neural development. We find that MIT exposure results in deficits in visually mediated avoidance behavior and increased susceptibility to seizures, as well electrophysiological abnormalities in optic tectal function, without Lck any effects on overall morphology, gross anatomy of the visual projections, overall visual function, and swimming ability. These effects indicate that chronic exposure to low levels of MIT results in neural circuit-level deficits that result in abnormal neurological function without causing increased mortality or even gross anatomical defects. Our findings, combined with the fact that the long-term neurological impacts of environmental exposure to MIT have not been determined, suggest a need for a closer evaluation of the safety of MIT in commercial and industrial products. (C) 2012 IBRO. Published by Elsevier Ltd. All rights reserved.