Anomalous spectral weight in photoemission spectra of the hole doped Haldane chain Y2-xSrxBaNiO5

In this paper, we present photoemission experiments on the hole doped Haldane chain compound $Y_{2-x}Sr_xBaNiO_5$. By using the photon energy dependence of the photoemission cross section, we identified the symmetry of the first ionisation states (d type). Hole doping in this system leads to a significant increase in the spectral weight at the top of the valence band without any change in the vicinity of the Fermi energy. This behavior, not observed in other charge transfer oxides at low doping level, could result from the inhomogeneous character of the doped system and from a Ni 3d-O 2p hybridization enhancement due to the shortening of the relevant Ni-O distance in the localized hole-doped regions.Comment: 5 pages, 4 figure

Random interactions and spin-glass thermodynamic transition in the hole-doped Haldane system Y2−x_{2-x}Cax_xBaNiO5_5

Magnetization, DC and AC bulk susceptibility of the $S$=1 Haldane chain system doped with electronic holes, Y$_{2-x}$Ca$_x$BaNiO$_5$ (0$\leq$x$\leq$0.20), have been measured and analyzed. The most striking results are (i) a sub-Curie power law behavior of the linear susceptibility, $\chi (T)$$\sim$ $T$$^{-\alpha}$, for temperature lower than the Haldane gap of the undoped compound (x=0) (ii) the existence of a spin-glass thermodynamic transition at $T$$_g$ = 2-3 K. These findings are consistent with (i) random couplings within the chains between the spin degrees of freedom induced by hole doping, (ii) the existence of ferromagnetic bonds that induce magnetic frustration when interchain interactions come into play at low temperature.Comment: 4 pages, 4 figures, to appear in Phys. Rev.

Simian Immunodeficiency Virus Replicates to High Levels in Naturally Infected African Green Monkeys without Inducing Immunologic or Neurologic Disease

African green monkeys can maintain long-term persistent infection with simian immunodeficiency viruses (SIVagm) without developing AIDS and thus provide an important model for understanding mechanisms of natural host resistance to disease. This study assessed the levels and anatomic distribution of SIVagm in healthy, naturally infected monkeys. Quantitative competitive reverse transcriptase PCR assays developed to measure SIVagm from two African green monkey subspecies demonstrated high levels of SIV RNA in plasma (>6 × 10(6) RNA copies/ml) in sabaeus and vervet monkeys. Infectious virus was readily recovered from plasma and peripheral blood mononuclear cells and shown to be highly cytopathic in human cell lines and macrophages. SIVagm DNA levels were highest in the gastrointestinal tract, suggesting that the gut is a major site for SIVagm replication in vivo. Appreciable levels of virus were also found within the brain parenchyma and the cerebrospinal fluid (CSF), with lower levels detected in peripheral blood cells and lymph nodes. Virus isolates from the CSF and brain parenchyma readily infected macrophages in culture, whereas lymph node isolates were more restricted to growth in human T-cell lines. Comparison of env V2-C4 sequences showed extensive amino acid diversity between SIVagm recovered from the central nervous system and that recovered from lymphoid tissues. Homology between brain and CSF viruses, macrophage tropism, and active replication suggest compartmentalization in the central nervous system without associated neuropathology in naturally infected monkeys. These studies provide evidence that the nonpathogenic nature of SIVagm in the natural host can be attributed neither to more effective host control over viral replication nor to differences in the tissue and cell tropism from those for human immunodeficiency virus type 1-infected humans or SIV-infected macaques

Molecular Pathways in Virus-Induced Cytokine Production

Virus infections induce a proinflammatory response including expression of cytokines and chemokines. The subsequent leukocyte recruitment and antiviral effector functions contribute to the first line of defense against viruses. The molecular virus-cell interactions initiating these events have been studied intensively, and it appears that viral surface glycoproteins, double-stranded RNA, and intracellular viral proteins all have the capacity to activate signal transduction pathways leading to the expression of cytokines and chemokines. The signaling pathways activated by viral infections include the major proinflammatory pathways, with the transcription factor NF-κB having received special attention. These transcription factors in turn promote the expression of specific inducible host proteins and participate in the expression of some viral genes. Here we review the current knowledge of virus-induced signal transduction by seven human pathogenic viruses and the most widely used experimental models for viral infections. The molecular mechanisms of virus-induced expression of cytokines and chemokines is also analyzed