<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Miorin, Lisa</style></author><author><style face="normal" font="default" size="100%">Albornoz, Amelina</style></author><author><style face="normal" font="default" size="100%">Baba, Marycelin M</style></author><author><style face="normal" font="default" size="100%">D'Agaro, Pierlanfranco</style></author><author><style face="normal" font="default" size="100%">Marcello, Alessandro</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Formation of membrane-defined compartments by tick-borne encephalitis virus contributes to the early delay in interferon signaling.</style></title><secondary-title><style face="normal" font="default" size="100%">Virus Res</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Virus Res.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Cell Membrane</style></keyword><keyword><style  face="normal" font="default" size="100%">Encephalitis Viruses, Tick-Borne</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Immune Evasion</style></keyword><keyword><style  face="normal" font="default" size="100%">Interferons</style></keyword><keyword><style  face="normal" font="default" size="100%">Receptors, Pattern Recognition</style></keyword><keyword><style  face="normal" font="default" size="100%">RNA, Viral</style></keyword><keyword><style  face="normal" font="default" size="100%">Signal Transduction</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2012</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2012 Feb</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">163</style></volume><pages><style face="normal" font="default" size="100%">660-6</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Interferons are key mediators of the innate antiviral response of the cell against viral infections. Viruses on the other hand have evolved various strategies to delay innate immunity in order to establish a productive infection. In this work we analyzed the pathway of interferon induction by the tick-borne encephalitis virus. We initially observed a consistent delay of interferon induction following virus replication. RIG-I, but not MDA5, and nuclear translocation of IRF3 were eventually required for interferon activation pointing to a defect in pattern recognition receptor's signaling. However, viral proteins could not directly inhibit the pathway suggesting an indirect mechanism. We found that dsRNA replication intermediates and replicated viral RNA localized to membrane-defined perinuclear compartments that resisted RNAse treatment. Thus, initial escape from innate immunity involved the formation of replication vesicles that may function as a barrier to pattern recognition receptors.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">2</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/22155022?dopt=Abstract</style></custom1></record></records></xml>