Increased number and function of natural killer cells in human immunodeficiency virus 1-positive subjects co-infected with herpes simplex virus 2

P>Natural killer (NK) cells bridge the interface between innate and adaptive immunity and are implicated in the control of herpes simplex virus 2 (HSV-2) infection. In subjects infected with human immunodeficiency virus 1 (HIV-1), the critical impact of the innate immune response on disease progression has recently come into focus. Higher numbers of NK cells are associated with lower HIV-1 plasma viraemia. Individuals with the compound genotype of killer cell immunoglobulin-like receptor (KIR) 3DS1 and human leucocyte antigen (HLA)-Bw4-80I, or who have alleles of KIR3DL1 that encode proteins highly expressed on the NK cell surface, have a significant delay in disease progression. We studied the effect of HSV-2 co-infection in HIV-1-infected subjects, and show that HSV-2 co-infection results in a pan-lymphocytosis, with elevated absolute numbers of CD4+ and CD8+ T cells, and NK cells. The NK cells in HSV-2 co-infected subjects functioned more efficiently, with an increase in degranulation after in vitro stimulation. The number of NK cells expressing the activating receptors NKp30 and NKp46, and expressing KIR3DL1 or KIR3DS1, was inversely correlated with HIV-1 plasma viral load in subjects mono-infected with HIV-1, but not in subjects co-infected with HSV-2. This suggests that HSV-2 infection mediates changes within the NK cell population that may affect immunity in HIV-1 infection.

A novel human CD4(+) T-cell inducer subset with potent immunostimulatory properties

The complexity of immunoregulation has focused attention on the CD4(+) T ""suppressor"" regulatory cell (T(reg)), which helps maintain balance between immunity and tolerance. An immunoregulatory T-cell population that upon activation amplifies cellular immune responses was described in murine models more than 30 years ago; however, no study has yet identified a naturally occurring T ""inducer"" cell type. Here, we report that the ectoenzyme CD39/NTPDase1 (ecto-nucleoside triphosphate diphosphohydrolase 1) helps to delineate a novel population of human ""inducer"" CD4(+) T cells (T(ind)) that significantly increases the proliferation and cytokine production of responder T cells in a dose-dependent manner. Furthermore, this unique T(ind) subset produces a distinct repertoire of cytokines in comparison to the other CD4(+) T-cell subsets. We propose that this novel CD4(+) T-cell population counterbalances the suppressive activity of suppressor T(reg) in peripheral blood and serves as a calibrator of immunoregulation.

Emily Kame Kngwarreye and the undeconstructible space of justice

Selected as part of an anthology featuring best or most representative of 20th century art writing. Other authors in anthology included Benjamin, Greenberg, Krauss, T.j. Clark, Roger Fry, Stuart Hall, etc. Intended as US textbook. My essay featured as part of study day on globalism in art at Tate Modern. Essay itself subject of PhD thesis by Sally Butler of EMSAH and other subsequent commentaries.

The Genome Sequence of Taurine Cattle: A Window to Ruminant Biology and Evolution

To understand the biology and evolution of ruminants, the cattle genome was sequenced to about sevenfold coverage. The cattle genome contains a minimum of 22,000 genes, with a core set of 14,345 orthologs shared among seven mammalian species of which 1217 are absent or undetected in noneutherian (marsupial or monotreme) genomes. Cattle-specific evolutionary breakpoint regions in chromosomes have a higher density of segmental duplications, enrichment of repetitive elements, and species-specific variations in genes associated with lactation and immune responsiveness. Genes involved in metabolism are generally highly conserved, although five metabolic genes are deleted or extensively diverged from their human orthologs. The cattle genome sequence thus provides a resource for understanding mammalian evolution and accelerating livestock genetic improvement for milk and meat production.

Effect of the microstructure on the lifetime of dental ceramics

Objectives. To evaluate the effect of the microstructure on the Weibull and slow crack growth (SCG) parameters and on the lifetime of three ceramics used as framework materials for fixed partial dentures (FPDs) (YZ - Vita In-Ceram YZ; IZ - Vita In-Ceram Zirconia; AL - Vita In-Ceram AL) and of two veneering porcelains (VM7 and VM9). Methods. Bar-shaped specimens were fabricated according to the manufacturer`s instructions. Specimens were tested in three-point flexure in 37 degrees C artificial saliva. Weibull analysis (n = 30) and a constant stress-rate test (n = 10) were used to determine the Weibull modulus (m) and SCG coefficient (n), respectively. Microstructural and fractographic analyzes were performed using SEM. ANOVA and Tukey`s test (alpha = 0.05) were used to statistically analyze data obtained with both microstructural and fractographic analyzes. Results. YZ and AL presented high crystalline content and low porosity (0.1-0.2%). YZ had the highest characteristic strength (sigma(0)) value (911 MPa) followed by AL (488 MPa) and IZ (423 MPa). Lower sigma(0) values were observed for the porcelains (68-75 MPa). Except for IZ and VM7, m values were similar among the ceramic materials. Higher n values were found for YZ (76) and AL (72), followed by IZ (54) and the veneering materials (36-44). Lifetime predictions showed that YZ was the material with the best mechanical performance. The size of the critical flaw was similar among the framework materials (34-48 mu m) and among the porcelains (75-86 mu m). Significance. The microstructure influenced the mechanical and SCG behavior of the studied materials and, consequently, the lifetime predictions. (C) 2011 Academy of Dental Materials. Published by Elsevier Ltd. All rights reserved.

Assembly and maturation of the flavivirus Kunjin virus appear to occur in the rough endoplasmic reticulum and along the secretory pathway, respectively

The intracellular assembly site for flaviviruses in currently not known but is presumed to be located within the lumen of the rough endoplasmic reticulum (RER), Building on previous studies involving immunofluorescence (IF) and cryoimmunoelectron microscopy of Kunjin virus (KUN)-infected cells, we sought to identify the steps involved in the assembly and maturation of KUN. Thus, using antibodies directed against envelope protein E in IF analysis, we found the accumulation of E within regions coincident with the RER and endosomal compartments. Immunogold labeling of cryosections of infected cells indicated that E and minor envelope protein prM were localized to reticulum membranes continuous with KUN-induced convoluted membranes (CM) or paracrystalline arrays (PC) and that sometimes the RER contained immunogold-labeled virus particles. Both proteins were also observed to be labeled in membranes at the periphery of the induced CIM or PC structures, but the latter were very seldom labeled internally. Utilizing drugs that inhibit protein and/or membrane traffic throughout the cell, we found that the secretion of KUN particles late in infection was significantly affected in the presence of brefeldin A and that the infectivity of secreted particles was severely affected in the presence of monensin and N-nonyl-deoxynojirimycin. Nocodazole did not appear to affect maturation, suggesting that microtubules play no role in assembly or maturation processes. Subsequently, we showed that the exit of intact virions from the RER involves the transport of individual virions within individual vesicles en route to the Golgi apparatus. The results suggest that the assembly of virions occurs within the lumen of the RER and that subsequent maturation occurs via the secretory pathway.