Disease relevance of Encephalomyocarditis Virus

• Activation of the translational suppressor 4E-BP1 following infection with encephalomyocarditis virus and poliovirus [1].
• Therapy with cyclosporine in experimental murine myocarditis with encephalomyocarditis virus [2].
• We investigated the effects of amlodipine on a murine model of congestive heart failure induced by the M variant of encephalomyocarditis virus (EMCV) [3].
• Vitamin B12 failed to inhibit translation by IRES elements from encephalomyocarditis virus (EMCV) or classical swine fever virus (CSFV) [4].
• We constructed a bicistronic retrovirus producing a single mRNA encoding both the therapeutic gene for the X-linked form of CGD (X-CGD), gp91phox, and the selectable human multidrug resistance gene, MDR1 linked together by the encephalomyocarditis virus internal ribosome entry site (IRES) [5].

High impact information on Encephalomyocarditis Virus

• Mice lacking p50 are unable effectively to clear L. monocytogenes and are more susceptible to infection with S. pneumoniae, but are more resistant to infection with murine encephalomyocarditis virus [6].
• In DBA/2 mice inoculated with the encephalomyocarditis virus, a more than 150% increase in myocardial serine elastase activity is observed [7].
• The IRF-1-/- mice were less resistant than normal mice to EMCV infection, as revealed by accelerated mortality and a larger virus titer in target organs [8].
• A A pyrimidine-rich stretch proximal to the initiation codon was also crucial for efficient translation of EMCV mRNA [9].
• The IL-8 inhibitory action on IFN-alpha antiviral activity was associated with reduced 2',5'-A oligoadenylate synthetase activity, a pathway well correlative with the anti- encephalomyocarditis virus action of IFN-alpha [10].

Chemical compound and disease context of Encephalomyocarditis Virus

• A foreign gene (bacterial chloramphenicol acetyltransferase, CAT) was inserted into pPNENPO cDNA between the PV and encephalomyocarditis virus IRES elements [11].
• Homologous recombination of this vector introduces a human gamma 1 constant-region sequence linked to the EMCV leader and a neomycin phosphotransferase (neo) gene [12].
• METHODS AND RESULTS: Four-week-old male DBA/2 mice were inoculated with EMCV and administered amlodipine, diltiazem, or vehicle PO for 2 weeks [3].
• As the result of PKR loss, they also showed impaired induction of IFN-alpha and IFN-beta genes in response to several inducers--specifically, encephalomyocarditis virus, lipopolysaccharide, and phorbol 12-myristate 13-acetate [13].
• Cynomolgus, rhesus, and Cebus monkeys failed to show glucose tolerance or insulin secretion abnormalities after infection with encephalomyocarditis virus or Coxsackie virus B4 [14].

Biological context of Encephalomyocarditis Virus

• Transgenic mice were generated using bicistronic transgenes with FGF-2 IRES or encephalomyocarditis virus (EMCV) IRES [15].
• In this report, we demonstrate that activation of phosphatidylinositol 3-kinase (PI3K) by either serum factors or IFNs blocks cell death induced by encephalomyocarditis virus (EMCV) and HSV [16].
• The presence of this chromosome in the hybrid cells was not sufficient, however, to confer antiviral resistance to the hybrids when they were treated with Mu-IFN-gamma and challenged with encephalomyocarditis virus [17].
• In our studies, we find that p50 is equally important in suppressing apoptosis during EMCV infection [18].
• Two members of the picornavirus family, encephalomyocarditis virus and poliovirus, inhibit phosphorylation of 4E-BP1 [19].

Anatomical context of Encephalomyocarditis Virus

• However, in rabbit reticulocyte lysates these same transcripts are translated from IC1 as well as from IC2, and transcripts in which m1 RNA is preceded by long sequences of encephalomyocarditis virus RNA (from the T7 polymerase-controlled pTM1 vector) are translated exclusively from IC1 [20].
• Inhibitory role of the host apoptogenic gene PKR in the establishment of persistent infection by encephalomyocarditis virus in U937 cells [21].
• Fibroblasts infected with EMCV (or treated with dsRNA) produced interleukin-6, an inflammatory and pyrogenic cytokine, in a p38 MAPK-dependent fashion [22].
• Effects of recombinant human leukocyte interferon alpha A/D on experimental myocarditis due to encephalomyocarditis virus were investigated [23].
• Interferon action: binding of viral RNA to the 40-kilodalton 2'-5'-oligoadenylate synthetase in interferon-treated HeLa cells infected with encephalomyocarditis virus [24].

Gene context of Encephalomyocarditis Virus

• Cell supernatants were harvested after 5-day incubation and assayed for IFN activity against encephalomyocarditis virus in human WISH cells [25].
• However, hu-IFN-gamma could not fully protect the clones from cytopathic effects of encephalomyocarditis virus and vesicular stomatitis virus while mo-IFN-gamma could [26].
• Accordingly, human cells in which PLSCR1 expression was decreased with short interfering RNA were rendered relatively insensitive to the antiviral activity of IFNs, resulting in higher titers of vesicular stomatitis virus (VSV) and encephalomyocarditis virus [27].
• However, these cells showed no antiviral protection in response to IFN-gamma when challenged with vesicular stomatitis virus (VSV) but limited protection when challenged with encephalomyocarditis virus (EMCV) [28].
• Moreover, cells expressing a low level of RLI (VAS3 and VAS 4) are partially resistant to EMCV infection [29].

Analytical, diagnostic and therapeutic context of Encephalomyocarditis Virus

• The eyes, kidneys and pancreas of mice (SJL/J) infected with encephalomyocarditis virus were examined by light and electron microscopy [30].
• RESULTS: In cell culture, using rl as the upstream gene, we demonstrate that the expression of the downstream tk gene is 12-fold greater using SIRES when compared with EMCV IRES [31].
• We intended to create an animal model for Reye's syndrome by treating mice with encephalomyocarditis virus, and/or salicylate, fructose, Atlox, butylated hydroxytoluene, pentachlorophenol, and an equal mixture of butylated hydroxytoluene and monosodium stearate [32].
• Immunofluorescence studies using specific antibodies demonstrated that p68 kinase which is distributed evenly in the cytoplasm of HeLa cells becomes concentrated around the nuclei after EMCV infection [33].
• The authors examined the susceptibility of five cell lines (WISH, HEp-2, Vero, A549, and WI-26VA4) to vesicular stomatitis virus (VSV) and encephalomyocarditis virus (EMCV), and compared the response of these cells to the inhibitory activity of IFN-alpha and IFN-gamma for the respective viral cytopathic effect (CPE) [34].

References