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encephalitis/phosphatase

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Protein phosphatase 1 (PP1) is a serine/threonine phosphatase which has been implicated in the regulation of a number of viruses, including HIV-1, Ebolavirus, and Rift Valley fever virus. Catalytic subunits of PP1 (PP1α, PP1β, and PP1γ) interact with a host of regulatory subunits and target a wide
Japanese encephalitis virus (JEV), a mosquito-borne flavivirus, causes acute encephalitis in humans with high mortality. Not much is known about the interactions between viral and cellular factors that regulate JEV infection. By using a kinase/phosphatase-wide RNAi screening approach, we identified

MicroRNA 155 regulates Japanese encephalitis virus-induced inflammatory response by targeting Src homology 2-containing inositol phosphatase 1.

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MicroRNAs (miRNAs) are single-stranded small RNA molecules that regulate various cellular processes. miRNA 155 (miR-155) regulates various aspects of innate and adaptive immune responses and plays a key role in various viral infections and the resulting neuroinflammation. The present study evaluated

Blocking of interferon-induced Jak-Stat signaling by Japanese encephalitis virus NS5 through a protein tyrosine phosphatase-mediated mechanism.

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Japanese encephalitis virus (JEV), a mosquito-borne flavivirus that causes severe human disease, has been shown to block the interferon (IFN)-induced Janus kinase signal transducer and activation of transcription (Jak-Stat) signaling cascade by preventing Tyk2 tyrosine phosphorylation and Stat

Susceptibility of naïve and differentiated PC12 cells to Japanese encephalitis virus infection.

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Japanese encephalitis is a mosquito-borne disease caused by Japanese encephalitis virus (JEV) infection. Although JEV infects and replicates in cells with multiple tissue origins, neurons are the preferential cells for JEV infection. Currently, the identities of JEV cell tropism are largely unclear.

Changes in the metabolic activity of macrophages under the influence of tick-borne encephalitis virus.

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The metabolic activity of macrophages infected with tick-borne encephalitis virus (TBEV) affecting the human nervous system has been studied for the first time. The penetration and reproduction of TBEV in the macrophages stimulated their oxygen metabolism, increasing the activity of NADPH-oxidase

Severe encephalitis in cynomolgus macaques exposed to aerosolized Eastern equine encephalitis virus.

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Cynomolgus macaques exposed to an aerosol containing a virulent strain of eastern equine encephalitis (EEE) virus developed neurological signs indicating encephalitis that corresponded with the onset of fever and an elevated heart rate. Viremia was either transient or undetectable even in animals

Acid phosphatase activity of cerebrospinal fluid cells in bacterial and abacterial meningitis.

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Acid phosphatase staining is performed on cerebrospinal fluid cells of 365 samples from 105 patients with various types of meningitis. This enzyme activity is strongly positive in the early samples of bacterial meningitis, as far as the patients had not received a pretreatment with antibiotics for

Dual-Specificity Phosphatase 4 Regulates STAT5 Protein Stability and Helper T Cell Polarization.

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Immune responses are critically regulated by the functions of CD4 helper T cells. Based on their secreted cytokines, helper T cells are further categorized into different subsets like Treg or Th17 cells, which suppress or promote inflammatory responses, respectively. Signals from IL-2 activate the

Immunohistochemical identification of caprine arthritis-encephalitis virus in paraffin-embedded specimens from naturally infected goats.

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The expression of caprine arthritis-encephalitis virus capsid protein was studied in seropositive naturally infected asymptomatic goals (10< seropositive naturally infected encephalitic kids (12) and goats (4), and noninfected control goats (3). Rabbit antiserum to recombinant viral capsid and

Natural infection of a great egret (Casmerodius albus) with eastern equine encephalitis virus.

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In July 2001, a great egret (Casmerodius albus) was found dead in Charlton County, Georgia (USA) and submitted to the Southeastern Cooperative Wildlife Disease Study (The University of Georgia, Athens, Georgia). Histopathologic findings included severe hepatic necrosis and necrosis of sheathed

Production of lethal infection that resembles fatal human disease by intranasal inoculation of macaques with Japanese encephalitis virus.

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Twelve rhesus macaques (Macaca mulatta) challenged intranasally with a wild-type Japanese encephalitis virus (JEV) developed clinical signs 11-14 days later. Tissues from the cerebral cortex, cerebellum, brainstem, thalamus, meninges, and all levels of the spinal cord were stained for JEV antigen

Dot-ELISA for serodiagnosis of human infections due to Western equine encephalitis virus.

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A standard dot-ELISA (enzyme-linked immunosorbent assay) was modified for use in detecting IgM and IgG class antibodies to Western equine encephalitis (WEE) virus in serum samples from humans infected with this virus. Nitrocellulose membranes were soaked in supernatant fluid from WEE virus-infected

Studies in the development of Japanese encephalitis vaccine: expression of virus envelope glycoprotein V3 (E) gene in yeast.

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A safe, effective and economical vaccine is required for the prevention of Japanese encephalitis (JE), a disease with high mortality and grave sequelae, which is prevalent in Japan and other countries in east, south-east and southern Asia. As the initial step to produce a second-generation vaccine,

Vascular and neuroglial changes in experimental herpes simplex encephalitis enzyme histochemical study.

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An enzyme histochemical study of experimental herpes simplex encephalitis of the mouse has revealed a decrease in the number of capillaries displaying alkaline phosphatase activity. Glial cells showed increased Inosine 5 diphosphatase and ATPase activity. These enzyme histochemical changes were
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