If C protein function is compromised, as in the case of F170S HPIV1, the resulting PKR activation and reduction in viral protein levels

enable the host to further reduce C protein levels and to mount a potent antiviral type I IFN response.”
“Gliotransmitters such as glutamate and ATP play an essential role in the prevention of the osmotic swelling of retinal ICG-001 glial (Muller) cells. It has been shown that vascular endothelial growth factor (VEGF) induces a Ca2+-dependent release of glutamate from the cells [Wurm et al. (2008), J Neurochem 104:386-399]. In the present study, we investigated with cell swelling experiments on freshly isolated retinal glial cells of the rat whether activation of voltage-gated Na+ (Na-v) and Ca2+ channels (VGCCs) is implicated

in mediating the VEGF-induced release of glutamate. We found that the inhibitory effect of VEGF on the osmotic swelling of retinal www.selleckchem.com/products/bindarit.html glial cells, used as an indicator of glutamate release, is prevented in the presence of selective blockers of T-type VGCCs (kurtoxin, mibefradil, Ni2+) and Na-v channels (TTX, saxitoxin, phenytoin). In contrast, the swelling-inhibitory effect of glutamate, that is mediated by a downstream release of ATP, remained unaffected in the presence of the blockers. The cells displayed immunolabeling for VGLUT3, Ca(v)1.2, Ca(v)3.1, and Na(v)1.6. In addition to VEGF, various other receptor agonists including neuropeptide Y, progesterone, erythropoietin, and endothelin-1 evoked a VGCC- and Na-v channel-dependent release of glutamate. It is concluded that activation of T-type VGCCs and Na-v channels is implicated in mediating the ligand-induced release of glutamate from retinal glial cells of the rat. The involvement of VLGUTs might suggest

that glutamate is released by vesicular exocytosis. (C) 2011 IBRO. Published by Elsevier Ltd. All rights reserved.”
“West Nile virus (WNV) is transmitted to vertebrate hosts primarily by infected Culex mosquitoes. Transmission of arboviruses by the bite of infected mosquitoes can potentiate infection in hosts Urease compared to viral infection by needle inoculation. Here we examined the effect of mosquito transmission on WNV infection and systematically investigated multiple factors that differ between mosquito infection and needle inoculation of WNV. We found that mice infected with WNV through the bite of a single infected Culex tarsalis mosquito exhibited 5- to 10-fold-higher viremia and tissue titers at 24 and 48 h postinoculation and faster neuroinvasion than mice given a median mosquito-inoculated dose of WNV (10(5) PFU) by needle. Mosquito-induced enhancement was not due to differences in inoculation location, because additional intravenous inoculation of WNV did not enhance viremia or tissue titers.